Skip to main content

Renal blood flow in sepsis



To assess changes in renal blood flow (RBF) in human and experimental sepsis, and to identify determinants of RBF.


Using specific search terms we systematically interrogated two electronic reference libraries to identify experimental and human studies of sepsis and septic acute renal failure in which RBF was measured. In the retrieved studies, we assessed the influence of various factors on RBF during sepsis using statistical methods.


We found no human studies in which RBF was measured with suitably accurate direct methods. Where it was measured in humans with sepsis, however, RBF was increased compared with normal. Of the 159 animal studies identified, 99 reported decreased RBF and 60 reported unchanged or increased RBF. The size of animal, technique of measurement, duration of measurement, method of induction of sepsis, and fluid administration had no effect on RBF. In contrast, on univariate analysis, state of consciousness of animals (P = 0.005), recovery after surgery (P < 0.001), haemodynamic pattern (hypodynamic or hyperdynamic state; P < 0.001) and cardiac output (P < 0.001) influenced RBF. However, multivariate analysis showed that only cardiac output remained an independent determinant of RBF (P < 0.001).


The impact of sepsis on RBF in humans is unknown. In experimental sepsis, RBF was reported to be decreased in two-thirds of studies (62 %) and unchanged or increased in one-third (38%). On univariate analysis, several factors not directly related to sepsis appear to influence RBF. However, multivariate analysis suggests that cardiac output has a dominant effect on RBF during sepsis, such that, in the presence of a decreased cardiac output, RBF is typically decreased, whereas in the presence of a preserved or increased cardiac output RBF is typically maintained or increased.


Acute renal failure (ARF) affects 5–7% of all hospitalized patients [13]. Sepsis and, in particular, septic shock are important risk factors for ARF in wards and remain the most important triggers for ARF in the intensive care unit (ICU) [48]. Among septic patients, the incidence of ARF is up to 51% [9] and that of severe ARF (i.e. ARF leading to the application of acute renal replacement therapy) is 5% [7, 10]. The mortality rate associated with severe ARF in the ICU setting remains high [25, 11].

A possible explanation for the high incidence and poor outcome of septic ARF relates to the lack of specific therapies. This, in turn, relates to our poor understanding of its pathogenesis. Nonetheless, a decrease in renal blood flow (RBF), causing renal ischaemia, has been proposed as central to the pathogenesis of septic ARF [1214]. However, the bulk of knowledge about RBF in sepsis is derived from animal studies using a variety of different models and techniques. This creates uncertainty regarding the applicability of these studies to humans. Furthermore, the findings of studies in which experimental sepsis was induced and RBF measured have not been systematically assessed. Accordingly, we obtained all electronically identifiable publications reporting RBF in sepsis and analyzed the data according to changes in RBF. We also studied the possible influences of several technical and model-related variables on RBF.

Materials and methods

We conducted a systematic interrogation of the literature using a standardized approach as described by Doig and Simpson [15] and Piper and coworkers [16]. We used two electronic reference libraries (Medline and PubMed), and searched for relevant articles using the following search terms: 'renal blood flow', 'kidney blood flow', 'renal blood supply', 'kidney blood supply', 'organ blood flow', 'organ blood supply', 'sepsis', 'septic shock', 'septicemia', 'caecal puncture ligation', 'cecum puncture ligation', 'lipopolysaccharide' and 'endotoxin'. We selected all animal studies published in the English language literature. Using the reference lists from each article, we identified and obtained other possible studies that might have reported information on RBF in septic ARF and that had not been identified by our electronic search strategy.

We assessed all human articles in detail. Because of the heterogeneity animal studies and the methods they employed, we also assessed all animal articles systematically for information on variables that might have influenced RBF in sepsis. The variables of interest were as follows: size of animal; technique of measurement for RBF (direct measurement via flow probe or microsphere technique or other technique); consciousness of animals during the study; recovery period between preparation surgery and the experiment; timing of RBF measurement in relation to septic insult; method used to induce sepsis (lipopolysaccharide [LPS], live bacteria, or caecal ligation–perforation technique); fluid administration during the experiment; cardiac output (CO); and haemodynamic patterns (hypodynamic and hyperdynamic sepsis).

Information obtained on RBF from these groups was compared. Comparisons were performed using the ?2 test or Fisher exact test where appropriate. Variables were also entered into a multivariate logistic regression analysis (MVLRA) model with RBF as the dependent variable. P < 0.05 was considered statistically significant.


Human studies

We found only three studies conducted in septic ICU patients in which RBF was measured [1719]. The findings of these studies suggest an increase in RBF during sepsis (Table 1). In only one patient was renal plasma flow (RPF) determined in the setting of oliguric ARF [19]. Such RPF was markedly increased at 2000 ml/min (normal 650 ml/min).

Table 1 Details of human studies conducted in septic patients measuring renal blood flow

Animal models

We found 159 [20178] animal studies that measured RBF in sepsis. Of these, 99 (62%) reported a decrease, whereas the remaining 60 (38%) studies reported no change or an increase in RBF (Table 2, Fig. 1).

Table 2 References for studies reporting various findings pertaining to RBF in experimental sepsis
Figure 1
figure 1

Effect of variables on renal blood flow: statistically significant findings. All of the differences between the shaded areas are statistically significant (P < 0.05). CO, cardiac output; inc, increased; RBF, renal blood flow; unc, unchanged.

Animal size

Experimental studies were conducted in a large variety of animals. We divided experimental animals into small (rats, mice, rabbits and piglets) and large (dogs, pigs and sheep). We identified 65 (41%) studies that were conducted in small animals and 94 (59%) that were conducted in large animals (Table 2). Of studies conducted in small animals, 46 found decreased and 19 (29%) unchanged or increased RBF. In large animals, 53 (56%) studies reported a decreased and 41 (44%) an unchanged or increased RBF (P = 0.066; Fig. 2).

Figure 2
figure 2

Effect of variables on renal blood flow: nonsignificant findings. None of the differences between and shaded areas are statistically significant. lps, lipopolysaccharide.

Technique for measuring renal blood flow

The techniques used for the measurement of RBF varied widely. Therefore, we compared studies using direct measurement of RBF via ultrasonic or electromagnetic flow probes ('direct' techniques) with measurement by microsphere technique or para-aminohippurate (PAH) clearance or other techniques such as measurement of blood velocity via video microscopy ('indirect' techniques). Of 80 studies using flow probes, 49 (61%) showed a decreased and 31 (39%) an unchanged or increased RBF (Table 2). Of 79 studies using other methods, 50 (63%) reported a decreased and 29 (37%) reported an unchanged or increased RBF (P = 0.791; Table 2, Fig. 2).

Consciousness of animals

The use of awake or unconscious animals might also have influenced RBF. For this reason, we compared studies using conscious with those using unconscious animals. Of 127 experiments conducted in unconscious animals (Table 2), 86 (68%) reported a decreased and 41 (32%) an unchanged or increased RBF. Of 32 studies conducted in conscious animals (Table 2), 13 (41 %) reported a decreased and 19 (59%) reported no change or an increase in RBF (P = 0.005; Fig. 1).

Recovery period between surgical preparation and actual experiment

Before conducting the experiments, a surgical procedure is typically needed to prepare the animals. We compared studies starting the experiment immediately after surgery with studies with a recovery period after anaesthesia. Of 33 studies with a recovery period (Table 2), 11 (33%) showed a decreased and 22 (67%) showed an unchanged or increased RBF. Of 126 studies without a recovery period (Table 2), 88 (70%) reported a decreased and 38 (30%) reported no change or an increase in RBF (P < 0.001; Fig. 1).

Time from septic insult

The duration of RBF observation after the septic insult varied widely. We divided the studies into those with a 'short' (<2 hours; early period after induction of sepsis) or 'long' (>2 hours; late period after the induction of sepsis) observation time. Among 47 experiments with short periods of observation after the induction of sepsis (Table 2), 32 (68%) showed a decreased and 15 (32%) showed an unchanged or increased RBF. Among the 112 experiments with long periods of observation after the induction of sepsis (Table 2), 67 (60%) showed a decreased and 45 (40%) showed an unchanged or increased RBF (P = 0.327; Fig. 2).

Methods of inducing sepsis

Many different methods of induction of sepsis were used. We compared LPS-induced sepsis with sepsis induced by injection of live bacteria or caecal ligation–perforation. Of 100 articles that used LPS (Table 2), 67 (67%) showed a decreased and 33 (33%) showed an unchanged or increased RBF. Among the other 59 studies (Table 2), 32 (54%) reported a reduced and 27 (46%) reported an unchanged or increased RBF (P = 0.109; Fig. 2).

Fluid administration

We compared studies according to whether there was fluid administration during the experiments. Thirty-four articles did not mention fluid administration. Among the 20 studies with no fluid administration (Table 2), 16 (80%) reported a decreased and 4 (20%) reported an unchanged or increased RBF. Of the 106 studies in which fluid was given (Table 2), 63 (59%) showed a decrease and 43 (41%) showed no change or an increase in RBF (P = 0.081; Fig. 2).

Haemodynamic patterns

Most septic patients exhibit a hyperdynamic state with elevated CO and decreased blood pressure, when CO is measured. Therefore, we compared studies in which animals had a hyperdynamic state (low peripheral vascular resistance [PVR]) of sepsis with studies in which this state was not present (normal or high PVR). There were 84 studies in which the hypodynamic versus hyperdynamic pattern could be assessed. Of 42 studies that fulfilled criteria for hypodynamic sepsis (Table 2), 38 (90%) showed a reduced and 4 (10%) showed no change or an increase in RBF. Of the 42 studies conducted in hyperdynamic sepsis (Table 2), 14 (33%) reported a decreased and 28 (67%) reported an unchanged or increased RBF (P < 0.001; Fig. 1).

Cardiac output

We compared those studies with increased or unchanged CO with studies with decreased CO. Some studies gave no indication of CO. Of the 51 studies with decreased CO (Table 2), 46 (90%) reported a decreased and 5 (10%) reported an unchanged or increased RBF. Among the 67 studies with an unchanged or increased CO (Table 2), 27 (40%) showed a reduced and 45 (60%) showed an unchanged or increased RBF (P < 0.001; Fig. 1).

Using MVLRA, we created a model to test for independent determinants of a RBF and found that only CO remained in the model (P < 0.001) as a significant predictor for RBF (Table 3).

Table 3 Multivariate logistic regression analysis of possible predictors of renal blood flow in experimental sepsis


We interrogated two electronic databases to assess the changes that occur in RBF during human and experimental sepsis in order to examine what might be the determinants of sepsis-associated changes in RBF. Variables that might influence RBF were used to categorize the heterogeneous data we found.

We found only a few human studies reporting RBF in a septic setting and found that the techniques used to measure RBF had poor accuracy and reproducibility. Only in a single patient with septic oliguric ARF was RBF measured. Nonetheless, within these serious limitations, we found that an increase in RBF was typically seen during sepsis.

We found that most animal studies reported a decrease in RBF in sepsis. However, we found that, in one-third of studies, RBF was either maintained or increased. We also found contradictory and inconsistent experimental findings with regard to RBF, which appeared to be affected by factors other than the induction of sepsis itself, including the consciousness of the animal, the recovery time after surgery and the haemodynamic pattern (hypodynamic or hyperdynamic state). More importantly, using MVLRA, we found that all of the above factors could be reduced to the dominant effect of CO on RBF. Thus, a low CO predicted a decreased RBF and a preserved or high CO predicted an unchanged or increased RBF. These findings are complex and require detailed discussion.

Human studies

Currently, only invasive techniques for measuring RBF have a high degree of accuracy. They require renal vein sampling. Because of the risks associated with such invasive measurement of RBF, only a few such studies have been conducted in humans with sepsis. Noninvasive methods of measurement such as the PAH clearance method are also possible but they assume a constant PAH extraction ratio of 0.91, such that RPF can be calculated with measurement of PAH concentrations in blood and urine. Unfortunately, the 'constant' PAH extraction ratio is not at all constant, is markedly unstable and is influenced by many factors, all of which apply in sepsis and ARF [18, 19]. Therefore, in order to achieve improved accuracy, this method must be made invasive by inserting a renal vein catheter in order to calculate the true PAH extraction ratio. The RPF measured by this method is called the true RPF. Finally, a third method uses a thermodilution renal vein catheter. RPF and RBF determined by the thermodilution method were reported to correlate with corrected PAH clearances (r = 0.79) [17].

However, a recently reported study [179] demonstrated that both methods have a low reproducibility and a within group error of up to 40%. Therefore, these methods are not sufficiently accurate to detect potentially important changes in RBF. Nonetheless, within the boundaries of the technology, true RPF measurements from human studies (Table 1) consistently suggest that renal blood flow is increased during human sepsis. In only one study [19] was RBF estimated in a septic patient with ARF. The RPF was found to be 2000 ml/min in this patient, which contrasts with the normal RPF in humans of 600–700 ml/min [180].

Animal models

Animal size

In small animals, RBFs values are very small (7.39 ml/min [40]). The changes estimated in different settings are even smaller (1.4 ml/min [40]). On the other hand, absolute blood flows in large animals are up to 250 times greater (330 ml/min [55]). We hypothesized that measurement accuracy might therefore change with animal size and lead to different observations. We found a strong trend in this direction, which just failed to achieve statistical significance.

Technique of measurement if renal blood flow

Using the flow probe technique, it is possible to measure the RBF continuously. Microsphere techniques are also accurate and can distinguish between cortical and medullar RBF, but using the latter technique it is only possible to take several 'snapshot views' of blood flow during the experiment. We hypothesized that the technique of measurement might have influenced findings. However, there was no significant difference between techniques.

Consciousness of animals

Most studies were conducted in unconscious animals. Within this group, RBF was significantly more likely to be decreased than in conscious animals. This effect might partly be explained by anaesthesia rather than sepsis itself. Our observations highlight this as an important area of concern in drawing conclusions about the effect of sepsis per se on RBF.

Time from septic insult

A recently published animal study [55] described the time-dependent development of hyperdynamic sepsis after live Escherichia coli injection. In that study the CO decreased immediately after injection, recovered and then increased by 2 hours until a hyperdynamic state was reached. Therefore, we divided the studies in experiments with less or greater than 2 hours of observation time after the septic insult in order to determine whether there were differences between early and late septic states. We hypothesized that studies with longer periods of observation after the insult (late sepsis) might show a different RBF. However, there was no difference between the two groups.

Recovery period

Surgical preparation was performed in many of the reviewed studies just before the experiments were started. The negative effect on RBF of immediately beginning the experiments after surgery might be explained by the prolonged anaesthesia time and the negative effect of anaesthesia. We found that lack of an adequate recovery period after surgical preparation increased the likelihood of RBF being decreased.

Method of inducing sepsis

Many different techniques are used to induce sepsis such as LPS injection, live bacteria injection and caecal ligation–perforation. Previous reports [181, 182] described a strong hypodynamic effect of injecting a bolus of LPS. Therefore, we hypothesized that studies using LPS might show decreased RBF. We found a trend in this direction that approached statistical significance.

Fluid administration

Most of the studies administered fluid during the experiments to counteract the hypotensive of effect of sepsis [14]. These fluids might maintain CO, central venous pressure and blood pressure, and thus affect RBF. As might be expected, we found a strong trend toward a higher RBF when fluid resuscitation was given, but this failed to achieve statistical significance.

Haemodynamic patterns

In septic patients, CO, blood pressure and PVR can be assessed. Most of these patients have an increased CO, a low blood pressure and a decreased PVR [14, 183189]. To assess what might happen to RBF in a haemodynamic situation simulating human sepsis, we compared studies with animals that had developed hyperdynamic sepsis (increased CO and decreased blood pressure) with those studies with hypodynamic sepsis (normal or increased PVR). Animals with hyperdynamic sepsis were more likely to exhibit preserved or increased RBF.

Cardiac output

In a recently published article [190] using a crossover animal model, CO was found to be the most important variable influencing organ blood flows. Thus, we compared studies showing an unchanged or increased CO with studies showing a decreased CO. We found a clear association between decreased CO and decreased RBF and between a preserved or increased CO and a preserved or increased RBF. Multivariate logistic analysis confirmed the role of CO as the most powerful independent predictor of RBF in sepsis (Table 2).


We only interrogated two English language electronic reference libraries and might have missed original contributions reported in other languages. However, we believe that it is unlikely that enough such studies would exist to change our conclusions materially.

In order to make comparisons, we categorized experiments according to pre-set criteria (small versus large animals, methods of induction of sepsis, high versus low CO, etc.) that we hypothesized, on grounds of biological plausibility, were likely to affect experimental findings. We acknowledge that such criteria are by definition arbitrary and the subject of individual judgement. Furthermore, other criteria that we did not consider could be tested. Nonetheless, we found that many of these criteria appeared to have some effect in reality. We also found that such effects appeared to be mostly related to their association with the CO state, which overwhelmingly was the only independent predictor in MVLRA for the outcome of RBF. We consider it unlikely that the choice of other criteria for comparison would materially affect our conclusions.

The observation time in the reviewed articles varied widely as well. We compared articles with a shorter period after the insult (2 hours) versus studies with a longer period of observation. We acknowledge that this division is artificial and might not truly reflect what happened, because some groups waited until the animal reached defined criteria before starting their observation time and others begun the observation immediately after the septic insult, making this variable extremely heterogeneous. Nonetheless, once again, given the overwhelming effect of CO on RBF, we consider that refinements to this criterion are unlikely to influence our conclusions.

Our observations suggest that the widely held paradigm that RBF decreases in sepsis [1214] and that such a decrease is responsible for the development of ARF is indeed sustained by the majority of studies. However, the reality beyond such a simplistic observation is much more complex. The animal studies are extraordinarily heterogeneous in their design and monitoring of RBF. Furthermore, the support that the bulk of the data offer to the concept of decreased RBF in sepsis is conditional upon a particular model of sepsis being present (hypodynamic sepsis without an increase in CO). If the CO is increased and PVR is decreased, then the most common finding is actually one of increased or preserved RBF. In the light of this review, we suggest that measurement of CO is a vital component of all future experimental studies measuring RBF in sepsis.

We note that, in human sepsis, systemic vasodilatation with a high CO is the dominant clinical finding. Such vasodilatation might also affect the afferent and efferent arterioles of the kidney. If the efferent arteriole dilated proportionately more than the afferent arteriole, then there would be a decrease in glomerular filtration pressure. This change in filtration pressure would decrease glomerular filtration rate and lead to oliguria and loss of small solute clearance. Accordingly, loss of glomerular filtration rate can occur with either vasoconstriction or vasodilatation.

Our findings have important implications for clinicians and for future strategies directed at preserving renal function in sepsis. They highlight the absence of human data. They show the heterogeneity and model dependence of the animal data. They also emphasize the limitations of the indirect data upon which clinical strategies are based. Much research remains to be done if we are to establish what happens to renal blood flow in human sepsis, and techniques are needed that permit such measurements to be taken noninvasively.


We interrogated the two major English language electronic reference libraries to examine changes in RBF in sepsis and septic ARF. We found that inadequate data exist to allow any conclusions to be drawn on the typical RBF or changes in RBF in humans. We also found that experimental data are extraordinarily heterogeneous in nature but show the dominant effect of CO on RBF, such that a low CO predicts a decreased RBF and an increased or preserved CO predicts an increased or preserved RBF. Given that CO is typically increased when measured in human sepsis in the ICU, the widely held paradigm that decreased RBF is pivotal to the pathogenesis of septic ARF might require reassessment.

Key messages

  • It is unknown whether RBF is increased, decreased, or unchanged in human sepsis.

  • Techniques to measure RBF in humans are invasive and of limited accuracy.

  • Data on RBF from animals are heterogenous and do not allow firm conclusions to be drawn.

  • RBF findings in experimental sepsis depend on the model used.

  • CO is the most important independent predictor of RBF in sepsis: if CO is increased, then RBF is typically increased; and if CO is decreased, the RBF is typically decreased.



acute renal failure


cardiac output


intensive care unit




multivariate logistic regression analysis




peripheral vascular resistance


renal blood flow


renal plasma flow.


  1. 1.

    Hou SH, Bushinsky DA, Wish JB, Cohen JJ, Harrington JT: Hospital-acquired renal insufficiency: a prospective study. Am J Med 1983, 74: 243-248. 10.1016/0002-9343(83)90618-6

    CAS  PubMed  Google Scholar 

  2. 2.

    Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. Am J Kidney Dis 2002, 39: 930-936. 10.1053/ajkd.2002.32766

    PubMed  Google Scholar 

  3. 3.

    Thadhani R, Pascual M, Bonventre JV: Acute renal failure. N Engl J Med 1996, 334: 1448-1460. 10.1056/NEJM199605303342207

    CAS  PubMed  Google Scholar 

  4. 4.

    Brivet FG, Kleinknecht DJ, Loirat P, Landais PJ: Acute renal failure in intensive care units: causes, outcome, and prognostic factors of hospital mortality; a prospective, multicenter study. French Study Group on Acute Renal Failure. Crit Care Med 1996, 24: 192-198. 10.1097/00003246-199602000-00003

    CAS  PubMed  Google Scholar 

  5. 5.

    Jorres A: Acute renal failure. Extracorporeal treatment strategies. Minerva Med 2002, 93: 329-324.

    CAS  PubMed  Google Scholar 

  6. 6.

    Liano F, Junco E, Pascual J, Madero R, Verde E: The spectrum of acute renal failure in the intensive care unit compared with that seen in other settings. The Madrid Acute Renal Failure Study Group. Kidney Int Suppl 1998, 66: S16-S24.

    CAS  PubMed  Google Scholar 

  7. 7.

    Silvester W, Bellomo R, Cole L: Epidemiology, management, and outcome of severe acute renal failure of critical illness in Australia. Crit Care Med 2001, 29: 1910-1915. 10.1097/00003246-200110000-00010

    CAS  PubMed  Google Scholar 

  8. 8.

    Uchino S, Doig GS, Bellomo R, Morimatsu H, Morgera S, Schetz M, Tan I, Bouman C, Nacedo E, Gibney N, et al.: Diuretics and mortality in acute renal failure. Crit Care Med 2004, 32: 1669-1677. 10.1097/01.CCM.0000132892.51063.2F

    PubMed  Google Scholar 

  9. 9.

    Rangel-Frausto MS, Pittet D, Costigan M, Hwang T, Davis CS, Wenzel RP: The natural history of the systemic inflammatory response syndrome (SIRS). A prospective study. JAMA 1995, 273: 117-123. 10.1001/jama.273.2.117

    CAS  PubMed  Google Scholar 

  10. 10.

    Cole L, Bellomo R, Baldwin I, Hayhoe M, Ronco C: The impact of lactate-buffered high-volume hemofiltration on acid-base balance. Intensive Care Med 2003, 29: 1113-1120. 10.1007/s00134-003-1812-1

    PubMed  Google Scholar 

  11. 11.

    Chew SL, Lins RL, Daelemans R, De Broe ME: Outcome in acute renal failure. Nephrol Dial Transplant 1993, 8: 101-107.

    CAS  PubMed  Google Scholar 

  12. 12.

    Badr KF: Sepsis-associated renal vasoconstriction: potential targets for future therapy. Am J Kidney Dis 1992, 20: 207-213.

    CAS  PubMed  Google Scholar 

  13. 13.

    De Vriese AS, Bourgeois M: Pharmacologic treatment of acute renal failure in sepsis. Curr Opin Crit Care 2003, 9: 474-480. 10.1097/00075198-200312000-00003

    PubMed  Google Scholar 

  14. 14.

    Schrier RW, Wang W: Acute renal failure and sepsis. N Engl J Med 2004, 351: 159-169. 10.1056/NEJMra032401

    CAS  PubMed  Google Scholar 

  15. 15.

    Doig GS, Simpson F: Efficient literature searching: a core skill for the practice of evidence-based medicine. Intensive Care Med 2003, 29: 2119-2127. 10.1007/s00134-003-1942-5

    PubMed  Google Scholar 

  16. 16.

    Piper RD, Cook DJ, Bone RC, Sibbald WJ: Introducing Critical Appraisal to studies of animal models investigating novel therapies in sepsis. Crit Care Med 1996, 24: 2059-2070. 10.1097/00003246-199612000-00021

    CAS  PubMed  Google Scholar 

  17. 17.

    Brenner M, Schaer GL, Mallory DL, Suffredini AF, Parrillo JE: Detection of renal blood flow abnormalities in septic and critically ill patients using a newly designed indwelling thermodilution renal vein catheter. Chest 1990, 98: 170-179.

    CAS  PubMed  Google Scholar 

  18. 18.

    Lucas CE, Rector FE, Werner M, Rosenberg IK: Altered renal homeostasis with acute sepsis. Clinical significance. Arch Surg 1973, 106: 444-449.

    CAS  PubMed  Google Scholar 

  19. 19.

    Rector F, Goyal S, Rosenberg IK, Lucas CE: Sepsis: a mechanism for vasodilatation in the kidney. Ann Surg 1973, 178: 222-226.

    PubMed Central  CAS  PubMed  Google Scholar 

  20. 20.

    Alden KJ, Motew SJ, Sharma AC, Ferguson JL: Effect of aminoguanidine on plasma nitric oxide by-products and blood flow during chronic peritoneal sepsis. Shock 1998, 9: 289-295.

    CAS  PubMed  Google Scholar 

  21. 21.

    Aranow JS, Wang H, Zhuang J, Fink MP: Effect of human hemoglobin on systemic and regional hemodynamics in a porcine model of endotoxemic shock. Crit Care Med 1996, 24: 807-814. 10.1097/00003246-199605000-00014

    CAS  PubMed  Google Scholar 

  22. 22.

    Auguste LJ, Stone AM, Wise L: The effects of Escherichia coli bacteremia on in vitro perfused kidneys. Ann Surg 1980, 192: 65-68.

    PubMed Central  CAS  PubMed  Google Scholar 

  23. 23.

    Beck RR, Abel FL, Papadakis E: Influence of ibuprofen on renal function in acutely endotoxemic dogs. Circ Shock 1989, 28: 37-47.

    CAS  PubMed  Google Scholar 

  24. 24.

    Begany DP, Carcillo JA, Herzer WA, Mi Z, Jackson EK: Inhibition of type IV phosphodiesterase by Ro 20-1724 attenuates endotoxin-induced acute renal failure. J Pharmacol Exp Ther 1996, 278: 37-41.

    CAS  PubMed  Google Scholar 

  25. 25.

    Bellomo R, Kellum JA, Pinsky MR: Transvisceral lactate fluxes during early endotoxemia. Chest 1996, 110: 198-204.

    CAS  PubMed  Google Scholar 

  26. 26.

    Bellomo R, Kellum JA, Wisniewski SR, Pinsky MR: Effects of norepinephrine on the renal vasculature in normal and endotoxemic dogs. Am J Respir Crit Care Med 1999, 159: 1186-1192.

    CAS  PubMed  Google Scholar 

  27. 27.

    Bloom IT, Bentley FR, Garrison RN: Escherichia coli bacteremia exacerbates cyclosporine-induced renal vasoconstriction. J Surg Res 1993, 54: 510-516. 10.1006/jsre.1993.1079

    CAS  PubMed  Google Scholar 

  28. 28.

    Boffa JJ, Just A, Coffman TM, Arendshorst WJ: Thromboxane receptor mediates renal vasoconstriction and contributes to acute renal failure in endotoxemic mice. J Am Soc Nephrol 2004, 15: 2358-2365. 10.1097/01.ASN.0000136300.72480.86

    CAS  PubMed  Google Scholar 

  29. 29.

    Bond RF: Peripheral vascular adrenergic depression during hypotension induced by E coli endotoxin. Adv Shock Res 1983, 9: 157-169.

    CAS  PubMed  Google Scholar 

  30. 30.

    Bone HG, Fischer SR, Schenarts PJ, McGuire R, Traber LD, Traber DL: Continuous infusion of pyridoxalated hemoglobin polyoxyethylene conjugate in hyperdynamic septic sheep. Shock 1998, 10: 69-76.

    CAS  PubMed  Google Scholar 

  31. 31.

    Bone HG, Schenarts PJ, Fischer SR, McGuire R, Traber LD, Traber DL: Pyridoxalated hemoglobin polyoxyethylene conjugate reverses hyperdynamic circulation in septic sheep. J Appl Physiol 1998, 84: 1991-1999.

    CAS  PubMed  Google Scholar 

  32. 32.

    Booke M, Hinder F, McGuire R, Traber LD, Traber DL: Nitric oxide synthase inhibition versus norepinephrine for the treatment of hyperdynamic sepsis in sheep. Crit Care Med 1996, 24: 835-844. 10.1097/00003246-199605000-00018

    CAS  PubMed  Google Scholar 

  33. 33.

    Booke M, Armstrong C, Hinder F, Conroy B, Traber LD, Traber DL: The effects of propofol on hemodynamics and renal blood flow in healthy and in septic sheep, and combined with fentanyl in septic sheep. Anesth Analg 1996, 82: 738-743. 10.1097/00000539-199604000-00011

    CAS  PubMed  Google Scholar 

  34. 34.

    Booke M, Hinder F, McGuire R, Traber LD, Traber DL: Nitric oxide synthase inhibition versus norepinephrine in ovine sepsis: effects on regional blood flow. Shock 1996, 5: 362-370.

    CAS  PubMed  Google Scholar 

  35. 35.

    Booke M, Hinder F, McGuire R, Traber LD, Traber DL: Selective inhibition of inducible nitric oxide synthase: effects on hemodynamics and regional blood flow in healthy and septic sheep. Crit Care Med 1999, 27: 162-167. 10.1097/00003246-199901000-00045

    CAS  PubMed  Google Scholar 

  36. 36.

    Booke M, Hinder F, McGuire R, Traber LD, Traber DL: Noradrenaline and nomega-monomethyl-L-arginine (L-NMMA): effects on haemodynamics and regional blood flow in healthy and septic sheep. Clin Sci (Lond) 2000, 98: 193-200.

    CAS  Google Scholar 

  37. 37.

    Breslow MJ, Miller CF, Parker SD, Walman AT, Traystman RJ: Effect of vasopressors on organ blood flow during endotoxin shock in pigs. Am J Physiol 1987, 252: H291-300.

    CAS  PubMed  Google Scholar 

  38. 38.

    Bressack MA, Morton NS, Hortop J: Group B streptococcal sepsis in the piglet: effects of fluid therapy on venous return, organ edema, and organ blood flow. Circ Res 1987, 61: 659-669.

    CAS  PubMed  Google Scholar 

  39. 39.

    Bronsveld W, van Lambalgen AA, van den Bos GC, Thijs LG, Koopman PA: Regional blood flow and metabolism in canine endotoxin shock before, during, and after infusion of glucose-insulin-potassium (GIK). Circ Shock 1986, 18: 31-42.

    CAS  PubMed  Google Scholar 

  40. 40.

    Burnier M, Waeber B, Aubert JF, Nussberger J, Brunner HR: Effects of nonhypotensive endotoxemia in conscious rats: role of prostaglandins. Am J Physiol 1988, 254: H509-H516.

    CAS  PubMed  Google Scholar 

  41. 41.

    Carroll GC, Snyder JV: Hyperdynamic severe intravascular sepsis depends on fluid administration in cynomolgus monkey. Am J Physiol 1982, 243: R131-R141.

    CAS  PubMed  Google Scholar 

  42. 42.

    Cavanagh D, Rao PS, Sutton DM, Bhagat BD, Bachmann F: Pathophysiology of endotoxin shock in the primate. Am J Obstet Gynecol 1970, 108: 705-722.

    CAS  PubMed  Google Scholar 

  43. 43.

    Cheng X, Pang CC: Pressor and vasoconstrictor effects of methylene blue in endotoxaemic rats. Naunyn Schmiedebergs Arch Pharmacol 1998, 357: 648-653.

    CAS  PubMed  Google Scholar 

  44. 44.

    Chin A, Radhakrishnan J, Fornell L, John E: Effects of tezosentan, a dual endothelin receptor antagonist, on the cardiovascular and renal systems of neonatal piglets during endotoxic shock. J Pediatr Surg 2002, 37: 482-487. 10.1053/jpsu.2002.30871

    PubMed  Google Scholar 

  45. 45.

    Chou DE, Cai H, Jayadevappa D, Porush JG: Regional expression of inducible nitric oxide synthase in the kidney stimulated by lipopolysaccharide in the rat. Exp Physiol 2002, 87: 153-162. 10.1113/eph8702289

    CAS  PubMed  Google Scholar 

  46. 46.

    Cohen RI, Hassell AM, Marzouk K, Marini C, Liu SF, Scharf SM: Renal effects of nitric oxide in endotoxemia. Am J Respir Crit Care Med 2001, 164: 1890-1895.

    CAS  PubMed  Google Scholar 

  47. 47.

    Cronenwett JL, Lindenauer SM: Distribution of intrarenal blood flow during bacterial sepsis. J Surg Res 1978, 24: 132-141. 10.1016/0022-4804(78)90165-8

    CAS  PubMed  Google Scholar 

  48. 48.

    Cronenwett JL, Lindenauer SM: Hemodynamic effects of cecal ligation sepsis in dogs. J Surg Res 1982, 33: 324-331. 10.1016/0022-4804(82)90045-2

    CAS  PubMed  Google Scholar 

  49. 49.

    Cryer HM, Unger LS, Garrison RN, Harris PD: Prostaglandins maintain renal microvascular blood flow during hyperdynamic bacteremia. Circ Shock 1988, 26: 71-88.

    CAS  PubMed  Google Scholar 

  50. 50.

    Cryer HG, Bloom IT, Unger LS, Garrison RN: Factors affecting renal microvascular blood flow in rat hyperdynamic bacteremia. Am J Physiol 1993, 264: H1988-H1997.

    CAS  PubMed  Google Scholar 

  51. 51.

    Cumming AD, Kline R, Linton AL: Association between renal and sympathetic responses to nonhypotensive systemic sepsis. Crit Care Med 1988, 16: 1132-1137.

    CAS  PubMed  Google Scholar 

  52. 52.

    Cumming AD, Driedger AA, McDonald JW, Lindsay RM, Solez K, Linton AL: Vasoactive hormones in the renal response to systemic sepsis. Am J Kidney Dis 1988, 11: 23-32.

    CAS  PubMed  Google Scholar 

  53. 53.

    Dedichen H, Schenk WG Jr: Hemodynamics of endotoxin shock in the dog. Arch Surg 1967, 95: 1013-1016.

    CAS  PubMed  Google Scholar 

  54. 54.

    Dedichen H: Hemodynamic changes in experimental endotoxin shock. Acta Chir Scand 1972, 138: 215-225.

    CAS  PubMed  Google Scholar 

  55. 55.

    Di Giantomasso D, May CN, Bellomo R: Vital organ blood flow during hyperdynamic sepsis. Chest 2003, 124: 1053-1059. 10.1378/chest.124.3.1053

    PubMed  Google Scholar 

  56. 56.

    Di Giantomasso D, May CN, Bellomo R: Norepinephrine and vital organ blood flow during experimental hyperdynamic sepsis. Intensive Care Med 2003, 29: 1774-1781. 10.1007/s00134-003-1736-9

    PubMed  Google Scholar 

  57. 57.

    Di Giantomasso D, Morimatsu H, May CN, Bellomo R: Intrarenal blood flow distribution in hyperdynamic septic shock: effect of norepinephrine. Crit Care Med 2003, 31: 2509-2513. 10.1097/01.CCM.0000084842.66153.5A

    CAS  PubMed  Google Scholar 

  58. 58.

    Doursout MF, Kilbourn RG, Hartley CJ, Chelly JE: Effects of N-methyl-L-arginine on cardiac and regional blood flow in a dog endotoxin shock model. J Crit Care 2000, 15: 22-29. 10.1053/jcrc.2000.0150022

    CAS  PubMed  Google Scholar 

  59. 59.

    Dziki AJ, Lynch WH, Ramsey CB, Law WR: Beta-adrenergic-dependent and -independent actions of naloxone on perfusion during endotoxin shock. Circ Shock 1993, 39: 29-38.

    CAS  PubMed  Google Scholar 

  60. 60.

    Emerson TE Jr, Wagner TD, Gill CC: In situ kidney pressure-flow-resistance relationship during endotoxin shock in dogs. Proc Soc Exp Biol Med 1966, 122: 366-368.

    PubMed  Google Scholar 

  61. 61.

    Etemadi AR, Tempel GE, Farah BA, Wise WC, Halushka PV, Cook JA: Beneficial effects of a leukotriene antagonist on endotoxin-induced acute hemodynamic alterations. Circ Shock 1987, 22: 55-63.

    CAS  PubMed  Google Scholar 

  62. 62.

    Fantini GA, Shiono S, Bal BS, Shires GT: Adrenergic mechanisms contribute to alterations in regional perfusion during normotensive E. coli bacteremia. J Trauma 1989, 29: 1252-1257.

    CAS  PubMed  Google Scholar 

  63. 63.

    Fink MP, Nelson R, Roethel R: Low-dose dopamine preserves renal blood flow in endotoxin shocked dogs treated with ibuprofen. J Surg Res 1985, 38: 582-591. 10.1016/0022-4804(85)90079-4

    CAS  PubMed  Google Scholar 

  64. 64.

    Fox GA, Lam CJ, Darragh WB, Neal AM, Inman KJ, Rutledge FS, Sibbald WJ: Circulatory sequelae of administering CPAP in hyperdynamic sepsis are time dependent. J Appl Physiol 1996, 81: 976-984.

    CAS  PubMed  Google Scholar 

  65. 65.

    Gardiner SM, Kemp PA, March JE, Bennett T: Influence of aminoguanidine and the endothelin antagonist, SB 209670, on the regional haemodynamic effects of endotoxaemia in conscious rats. Br J Pharmacol 1996, 118: 1822-1828.

    PubMed Central  CAS  PubMed  Google Scholar 

  66. 66.

    Gardiner SM, Kemp PA, March JE, Bennett T: Regional haemodynamic responses to infusion of lipopolysaccharide in conscious rats: effects of pre- or post-treatment with glibenclamide. Br J Pharmacol 1999, 128: 1772-1778. 10.1038/sj.bjp.0702985

    PubMed Central  CAS  PubMed  Google Scholar 

  67. 67.

    Garrison RN, Wilson MA, Matheson PJ, Spain DA: Nitric oxide mediates redistribution of intrarenal blood flow during bacteremia. J Trauma 1995, 39: 90-96. discussion 96-97.

    CAS  PubMed  Google Scholar 

  68. 68.

    Gullichsen E, Nelimarkka O, Halkola L, Niinikoski J: Renal oxygenation in endotoxin shock in dogs. Crit Care Med 1989, 17: 547-550.

    CAS  PubMed  Google Scholar 

  69. 69.

    Gullichsen E: Renal perfusion and metabolism in experimental endotoxin shock. Acta Chir Scand Suppl 1991, 560: 7-31.

    CAS  PubMed  Google Scholar 

  70. 70.

    Guntheroth WG, Hougen T, Kaplan EL: Absence of pooling with endotoxin shock in the canine kidney. J Appl Physiol 1972, 32: 512-515.

    CAS  PubMed  Google Scholar 

  71. 71.

    Hallemeesch MM, Cobben DC, Dejong CH, Soeters PB, Deutz NE: Renal amino acid metabolism during endotoxemia in the rat. J Surg Res 2000, 92: 193-200. 10.1006/jsre.2000.5867

    CAS  PubMed  Google Scholar 

  72. 72.

    Hallemeesch MM, Soeters PB, Deutz NE: Renal arginine and protein synthesis are increased during early endotoxemia in mice. Am J Physiol Renal Physiol 2002, 282: F316-F323.

    PubMed  Google Scholar 

  73. 73.

    Haybron DM, Townsend MC, Hampton WW, Schirmer JM, Fry DE: Effective renal blood flow and renal energy charge in murine peritonitis. Am Surg 1986, 52: 625-629.

    CAS  PubMed  Google Scholar 

  74. 74.

    Haybron DM, Townsend MC, Hampton WW, Schirmer WJ, Schirmer JM, Fry DE: Alterations in renal perfusion and renal energy charge in murine peritonitis. Arch Surg 1987, 122: 328-331.

    CAS  PubMed  Google Scholar 

  75. 75.

    Haywood GA, Tighe D, Moss R, al-Saady N, Foshola TO, Riley SP, Pearson I, Webb A, McKenna WJ, Bennett ED: Goal directed therapy with dobutamine in a porcine model of septic shock: effects on systemic and renal oxygen transport. Postgrad Med J 1991, S36-S39. discussion S40-S41

    Google Scholar 

  76. 76.

    Hazelzet JA, Stubenitsky R, Petrov AB, van Wieringen GW, van der Voort E, Hess J, Hop WC, Thijs LG, Duncker DJ, Poolman JT, et al.: Cardiovascular aspects of experimental meningococcal sepsis in young and older awake piglets: age-related differences. Shock 1999, 12: 145-154.

    CAS  PubMed  Google Scholar 

  77. 77.

    Heemskerk AE, Huisman E, van Lambalgen AA, Appelmelk BJ, van den Bos GC, Thijs LG, Tangelder GJ: Gram-negative shock in rats depends on the presence of capsulated bacteria and is modified by laparotomy. Shock 1996, 6: 418-425.

    CAS  PubMed  Google Scholar 

  78. 78.

    Heemskerk AE, Huisman E, van Lambalgen AA, van den Bos GC, Hennekes M, Thijs LG, Tangelder GJ: Renal function and oxygen consumption during bacteraemia and endotoxaemia in rats. Nephrol Dial Transplant 1997, 12: 1586-1594. 10.1093/ndt/12.8.1586

    CAS  PubMed  Google Scholar 

  79. 79.

    Henderson JL, Statman R, Cunningham JN, Cheng W, Damiani P, Siconolfi A, Horovitz JH: The effects of nitric oxide inhibition on regional hemodynamics during hyperdynamic endotoxemia. Arch Surg 1994, 129: 1271-1274. discussion 1275

    CAS  PubMed  Google Scholar 

  80. 80.

    Henrich WL, Hamasaki Y, Said SI, Campbell WB, Cronin RE: Dissociation of systemic and renal effects in endotoxemia. Prostaglandin inhibition uncovers an important role of renal nerves. J Clin Invest 1982, 69: 691-699.

    PubMed Central  CAS  PubMed  Google Scholar 

  81. 81.

    Hermreck AS, Thal AP: Mechanisms for the high circulatory requirements in sepsis and septic shock. Ann Surg 1969, 170: 677-695.

    PubMed Central  CAS  PubMed  Google Scholar 

  82. 82.

    Heyman SN, Darmon D, Goldfarb M, Bitz H, Shina A, Rosen S, Brezis M: Endotoxin-induced renal failure. I. A role for altered renal microcirculation. Exp Nephrol 2000, 8: 266-274. 10.1159/000020678

    CAS  PubMed  Google Scholar 

  83. 83.

    Hiltebrand LB, Krejci V, Banic A, Erni D, Wheatley AM, Sigurdsson GH: Dynamic study of the distribution of microcirculatory blood flow in multiple splanchnic organs in septic shock. Crit Care Med 2000, 28: 3233-3241. 10.1097/00003246-200009000-00019

    CAS  PubMed  Google Scholar 

  84. 84.

    Hiltebrand LB, Krejci V, Sigurdsson GH: Effects of dopamine, dobutamine, and dopexamine on microcirculatory blood flow in the gastrointestinal tract during sepsis and anesthesia. Anesthesiology 2004, 100: 1188-1197. 10.1097/00000542-200405000-00022

    CAS  PubMed  Google Scholar 

  85. 85.

    Hinshaw LB, Solomon LA, Holmes DD, Greenfield LJ: Comparison of canine responses to Escherichia coli organisms and endotoxin. Surg Gynecol Obstet 1968, 127: 981-988.

    CAS  PubMed  Google Scholar 

  86. 86.

    Hussain SN, Roussos C: Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs. J Appl Physiol 1985, 59: 1802-1808.

    CAS  PubMed  Google Scholar 

  87. 87.

    Jepson MM, Cox M, Bates PC, Rothwell NJ, Stock MJ, Cady EB, Millward DJ: Regional blood flow and skeletal muscle energy status in endotoxemic rats. Am J Physiol 1987, 252: E581-E587.

    CAS  PubMed  Google Scholar 

  88. 88.

    Keeler R, Barrientos A, Lee K: Circulatory effects of acute or chronic endotoxemia in rats. Can J Physiol Pharmacol 1981, 59: 204-208.

    CAS  PubMed  Google Scholar 

  89. 89.

    Kellum JA, Bellomo R, Kramer DJ, Pinsky MR: Hepatic anion flux during acute endotoxemia. J Appl Physiol 1995, 78: 2212-2217.

    CAS  PubMed  Google Scholar 

  90. 90.

    Kikeri D, Pennell JP, Hwang KH, Jacob AI, Richman AV, Bourgoignie JJ: Endotoxemic acute renal failure in awake rats. Am J Physiol 1986, 250: F1098-F1106.

    CAS  PubMed  Google Scholar 

  91. 91.

    Kirkebo A, Tyssebotn I: Renal blood flow distribution during E. coli endotoxin shock in dog. Acta Physiol Scand 1980, 108: 367-372.

    CAS  PubMed  Google Scholar 

  92. 92.

    Knight RJ, Bowmer CJ, Yates MS: Effect of the selective A1 adenosine antagonist 8-cyclopentyl-1,3-dipropylxanthine on acute renal dysfunction induced by Escherichia coli endotoxin in rats. J Pharm Pharmacol 1993, 45: 979-984.

    CAS  PubMed  Google Scholar 

  93. 93.

    Knotek M, Rogachev B, Wang W, Ecder T, Melnikov V, Gengaro PE, Esson M, Edelstein CL, Dinarello CA, Schrier RW: Endotoxemic renal failure in mice: role of tumor necrosis factor independent of inducible nitric oxide synthase. Kidney Int 2001, 59: 2243-2249.

    CAS  PubMed  Google Scholar 

  94. 94.

    Knuth OE, Wagenknecht LV, Madsen PO: The effect of various treatments on renal function during endotoxin shock. An experimental study in dogs. Invest Urol 1972, 9: 304-309.

    CAS  PubMed  Google Scholar 

  95. 95.

    Koyama S: Participation of central alpha-receptors on hemodynamic response to E. coli endotoxin. Am J Physiol 1984, 247: R655-R662.

    CAS  PubMed  Google Scholar 

  96. 96.

    Kreimeier U, Hammersen F, Ruiz-Morales M, Yang Z, Messmer K: Redistribution of intraorgan blood flow in acute, hyperdynamic porcine endotoxemia. Eur Surg Res 1991, 23: 85-99.

    CAS  PubMed  Google Scholar 

  97. 97.

    Kreimeier U, Brueckner UB, Gerspach S, Veitinger K, Messmer K: A porcine model of hyperdynamic endotoxemia: pattern of respiratory, macrocirculatory, and regional blood flow changes. J Invest Surg 1993, 6: 143-156.

    CAS  PubMed  Google Scholar 

  98. 98.

    Krejci V, Hiltebrand LB, Erni D, Sigurdsson GH: Endothelin receptor antagonist bosentan improves microcirculatory blood flow in splanchnic organs in septic shock. Crit Care Med 2003, 31: 203-210. 10.1097/00003246-200301000-00031

    CAS  PubMed  Google Scholar 

  99. 99.

    Krysztopik RJ, Bentley FR, Spain DA, Wilson MA, Garrison RN: Free radical scavenging by lazaroids improves renal blood flow during sepsis. Surgery 1996, 120: 657-662.

    CAS  PubMed  Google Scholar 

  100. 100.

    Krysztopik RJ, Bentley FR, Wilson MA, Spain DA, Garrison RN: Vasomotor response to pentoxifylline mediates improved renal blood flow to bacteremia. J Surg Res 1996, 63: 17-22. 10.1006/jsre.1996.0215

    CAS  PubMed  Google Scholar 

  101. 101.

    Laesser M, Oi Y, Ewert S, Fandriks L, Aneman A: The angiotensin II receptor blocker candesartan improves survival and mesenteric perfusion in an acute porcine endotoxin model. Acta Anaesthesiol Scand 2004, 48: 198-204. 10.1111/j.0001-5172.2004.00283.x

    CAS  PubMed  Google Scholar 

  102. 102.

    Lang CH, Bagby GJ, Ferguson JL, Spitzer JJ: Cardiac output and redistribution of organ blood flow in hypermetabolic sepsis. Am J Physiol 1984, 246: R331-R337.

    CAS  PubMed  Google Scholar 

  103. 103.

    Law WR, Ferguson JL: Naloxone alters organ perfusion during endotoxin shock in conscious rats. Am J Physiol 1988, 255: H1106-H1113.

    CAS  PubMed  Google Scholar 

  104. 104.

    Levy B, Mansart A, Bollaert PE, Franck P, Mallie JP: Effects of epinephrine and norepinephrine on hemodynamics, oxidative metabolism, and organ energetics in endotoxemic rats. Intensive Care Med 2003, 29: 292-300.

    PubMed  Google Scholar 

  105. 105.

    Levy B, Vallee C, Lauzier F, Plante GE, Mansart A, Mallie JP, Lesur O: Comparative effects of vasopressin, norepinephrine, and L-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock. Am J Physiol Heart Circ Physiol 2004, 287: H209-H215. 10.1152/ajpheart.00946.2003

    CAS  PubMed  Google Scholar 

  106. 106.

    Linder MM, Hartel W, Alken P, Muschaweck R: Renal tissue oxygen tension during the early phase of canine endotoxin shock. Surg Gynecol Obstet 1974, 138: 171-173.

    CAS  PubMed  Google Scholar 

  107. 107.

    Lindgren S, Almqvist P, Arvidsson D, Montgomery A, Andersson KE, Haglund U: Lack of beneficial effects of milrinone in severe septic shock. Circ Shock 1990, 31: 365-375.

    CAS  PubMed  Google Scholar 

  108. 108.

    Lingnau W, McGuire R, Booke M, Traber LD, Traber DL: Effects of alpha-trinositol on systemic inflammation and renal function in ovine bacterial sepsis. Shock 1997, 8: 179-185.

    CAS  PubMed  Google Scholar 

  109. 109.

    Lugon JR, Boim MA, Ramos OL, Ajzen H, Schor N: Renal function and glomerular hemodynamics in male endotoxemic rats. Kidney Int 1989, 36: 570-575.

    CAS  PubMed  Google Scholar 

  110. 110.

    Maitra SR, Homan CS, Pan W, Geller ER, Henry MC, Thode HC Jr: Renal gluconeogenesis and blood flow during endotoxic shock. Acad Emerg Med 1996, 3: 1006-1010.

    CAS  PubMed  Google Scholar 

  111. 111.

    Malay MB, Ashton JL, Dahl K, Savage EB, Burchell SA, Ashton RC Jr, Sciacca RR, Oliver JA, Landry DW: Heterogeneity of the vasoconstrictor effect of vasopressin in septic shock. Crit Care Med 2004, 32: 1327-1331. 10.1097/01.CCM.0000128578.37822.F1

    CAS  PubMed  Google Scholar 

  112. 112.

    Martin CM, Sibbald WJ: Modulation of hemodynamics and organ blood flow by nitric oxide synthase inhibition is not altered in normotensive, septic rats. Am J Respir Crit Care Med 1994, 150: 1539-1544.

    CAS  PubMed  Google Scholar 

  113. 113.

    Mellins RB, Levine OR, Wigger HJ, Leidy G, Curnen EC: Experimental menigococcemia: model of overwhelming infection in unanesthetized monkeys. J Appl Physiol 1972, 32: 309-314.

    CAS  PubMed  Google Scholar 

  114. 114.

    Meyer J, Hinder F, Stothert J Jr, Traber LD, Herndon DN, Flynn JT, Traber DL: Increased organ blood flow in chronic endotoxemia is reversed by nitric oxide synthase inhibition. J Appl Physiol 1994, 76: 2785-2793.

    CAS  PubMed  Google Scholar 

  115. 115.

    Millar CG, Thiemermann C: Intrarenal haemodynamics and renal dysfunction in endotoxaemia: effects of nitric oxide synthase inhibition. Br J Pharmacol 1997, 121: 1824-1830.

    PubMed Central  CAS  PubMed  Google Scholar 

  116. 116.

    Millar CG, Thiemermann C: Carboxy-PTIO, a scavenger of nitric oxide, selectively inhibits the increase in medullary perfusion and improves renal function in endotoxemia. Shock 2002, 18: 64-68. 10.1097/00024382-200207000-00012

    PubMed  Google Scholar 

  117. 117.

    Miller RL, Forsyth RP, Hoffbrand BI, Melmon KL: Cardiovascular effects of hemorrhage during endotoxemia in unanesthetized monkeys. Am J Physiol 1973, 224: 1087-1091.

    CAS  PubMed  Google Scholar 

  118. 118.

    Mitaka C, Hirata Y, Yokoyama K, Nagura T, Tsunoda Y, Amaha K: Improvement of renal dysfunction in dogs with endotoxemia by a nonselective endothelin receptor antagonist. Crit Care Med 1999, 27: 146-153. 10.1097/00003246-199901000-00043

    CAS  PubMed  Google Scholar 

  119. 119.

    Morisaki H, Sibbald W, Martin C, Doig G, Inman K: Hyperdynamic sepsis depresses circulatory compensation to normovolemic anemia in conscious rats. J Appl Physiol 1996, 80: 656-664.

    CAS  PubMed  Google Scholar 

  120. 120.

    Mulder MF, van Lambalgen AA, van Kraats AA, Scheffer PG, Bouman AA, van den Bos GC, Thijs LG: Systemic and regional hemodynamic changes during endotoxin or platelet activating factor (PAF)-induced shock in rats. Circ Shock 1993, 41: 221-229.

    CAS  PubMed  Google Scholar 

  121. 121.

    Mulder MF, van Lambalgen AA, van den Bos GC, Thijs LG: The fall of cardiac output in endotoxemic rats cannot explain all changes in organ blood flow: a comparison between endotoxin and low venous return shock. Shock 1996, 5: 135-140.

    CAS  PubMed  Google Scholar 

  122. 122.

    Murphey ED, Traber DL: Cardiopulmonary and splanchnic blood flow during 48 hours of a continuous infusion of endotoxin in conscious pigs: a model of hyperdynamic shock. Shock 2000, 13: 224-229.

    CAS  PubMed  Google Scholar 

  123. 123.

    Nishijima MK, Breslow MJ, Miller CF, Traystman RJ: Effect of naloxone and ibuprofen on organ blood flow during endotoxic shock in pig. Am J Physiol 1988, 255: H177-H184.

    CAS  PubMed  Google Scholar 

  124. 124.

    Nishiyama A, Miura K, Miyatake A, Fujisawa Y, Yue W, Fukui T, Kimura S, Abe Y: Renal interstitial concentration of adenosine during endotoxin shock. Eur J Pharmacol 1999, 385: 209-216. 10.1016/S0014-2999(99)00716-5

    CAS  PubMed  Google Scholar 

  125. 125.

    Offner PJ, Robertson FM, Pruitt BA Jr: Effects of nitric oxide synthase inhibition on regional blood flow in a porcine model of endotoxic shock. J Trauma 1995, 39: 338-343.

    CAS  PubMed  Google Scholar 

  126. 126.

    O'Hair DP, Adams MB, Tunberg TC, Osborn JL: Relationships among endotoxemia, arterial pressure, and renal function in dogs. Circ Shock 1989, 27: 199-210.

    PubMed  Google Scholar 

  127. 127.

    Oldner A, Konrad D, Weitzberg E, Rudehill A, Rossi P, Wanecek M: Effects of levosimendan, a novel inotropic calcium-sensitizing drug, in experimental septic shock. Crit Care Med 2001, 29: 2185-2193. 10.1097/00003246-200111000-00022

    CAS  PubMed  Google Scholar 

  128. 128.

    Ottosson J, Dawidson I, Brandberg A, Idvall J, Sandor Z: Cardiac output and organ blood flow in experimental septic shock: effect of treatment with antibiotics, corticosteroids, and fluid infusion. Circ Shock 1991, 35: 14-24.

    CAS  PubMed  Google Scholar 

  129. 129.

    Oyama T, Toyooka K, Sato Y, Kondo S, Kudo T: Effect of endotoxic shock on renal and hormonal functions. Can Anaesth Soc J 1978, 25: 380-391.

    CAS  PubMed  Google Scholar 

  130. 130.

    Passmore JC, Neiberger RE, Eden SW: Measurement of intrarenal anatomic distribution of krypton-85 in endotoxic shock in dogs. Am J Physiol 1977, 232: H54-H58.

    CAS  PubMed  Google Scholar 

  131. 131.

    Pastor CM: Vascular hyporesponsiveness of the renal circulation during endotoxemia in anesthetized pigs. Crit Care Med 1999, 27: 2735-2740. 10.1097/00003246-199912000-00022

    CAS  PubMed  Google Scholar 

  132. 132.

    Preiser JC, Sun Q, Hadj-Sadok D, Vincent JL: Differential effects of a selective inhibitor of soluble guanylyl cyclase on global and regional hemodynamics during canine endotoxic shock. Shock 2003, 20: 465-468. 10.1097/01.shk.0000092267.01859.e9

    CAS  PubMed  Google Scholar 

  133. 133.

    Prins HA, Houdijk AP, Wiezer MJ, Teerlink T, van Lambalgen AA, Thijs LG, van Leeuwen PA: The effect of mild endotoxemia during low arginine plasma levels on organ blood flow in rats. Crit Care Med 2000, 28: 1991-1997. 10.1097/00003246-200006000-00051

    CAS  PubMed  Google Scholar 

  134. 134.

    Rao PS, Bhagat B: Effect of dopamine on renal blood flow of baboon in endotoxin shock. Pflugers Arch 1978, 374: 105-106. 10.1007/BF00585704

    CAS  PubMed  Google Scholar 

  135. 135.

    Rao PS, Cavanagh D, Marsden KA, Knuppel RA, Spaziani E: Prostaglandin D2 in canine endotoxic shock. Hemodynamic, hematologic, biochemical, and blood gas analyses. Am J Obstet Gynecol 1984, 148: 964-972.

    CAS  PubMed  Google Scholar 

  136. 136.

    Rao PS, Cavanagh DM, Fiorica JV, Spaziani E: Endotoxin-induced alterations in renal function with particular reference to tubular enzyme activity. Circ Shock 1990, 31: 333-342.

    CAS  PubMed  Google Scholar 

  137. 137.

    Raper RF, Sibbald WJ, Hobson J, Rutledge FS: Effect of PGE1 on altered distribution of regional blood flows in hyperdynamic sepsis. Chest 1991, 100: 1703-1711.

    CAS  PubMed  Google Scholar 

  138. 138.

    Ravikant T, Lucas CE: Renal blood flow distribution in septic hyperdynamic pigs. J Surg Res 1977, 22: 294-298. 10.1016/0022-4804(77)90146-9

    CAS  PubMed  Google Scholar 

  139. 139.

    Sam AD II, Sharma AC, Rice AN, Ferguson JL, Law WR: Adenosine and nitric oxide regulate regional vascular resistance via interdependent and independent mechanisms during sepsis. Crit Care Med 2000, 28: 1931-1939. 10.1097/00003246-200006000-00041

    PubMed  Google Scholar 

  140. 140.

    Schaer GL, Fink MP, Chernow B, Ahmed S, Parrillo JE: Renal hemodynamics and prostaglandin E2 excretion in a nonhuman primate model of septic shock. Crit Care Med 1990, 18: 52-59.

    CAS  PubMed  Google Scholar 

  141. 141.

    Schirmer WJ, Schirmer JM, Naff GB, Fry DE: Systemic complement activation produces hemodynamic changes characteristic of sepsis. Arch Surg 1988, 123: 316-321.

    CAS  PubMed  Google Scholar 

  142. 142.

    Selmyer JP, Reynolds DG, Swan KG: Renal blood flow during endotoxin shock in the subhuman primate. Surg Gynecol Obstet 1973, 137: 2-6.

    CAS  PubMed  Google Scholar 

  143. 143.

    Shanbour LL, Lindeman RD, Archer LT, Tung SH, Hinshaw LB: Improvement of renal hemodynamics in endotoxin shock with dopamine, phenoxybenzamine and dextran. J Pharmacol Exp Ther 1971, 176: 383-388.

    CAS  PubMed  Google Scholar 

  144. 144.

    Somani P, Saini RK: A comparison of the cardiovascular, renal, and coronary effects of dopamine and monensin in endotoxic shock. Circ Shock 1981, 8: 451-464.

    CAS  PubMed  Google Scholar 

  145. 145.

    Spain DA, Wilson MA, Garrison RN: Nitric oxide synthase inhibition exacerbates sepsis-induced renal hypoperfusion. Surgery 1994, 116: 322-330. discussion 330-321

    CAS  PubMed  Google Scholar 

  146. 146.

    Stone AM, Stein T, LaFortune J, Wise L: Effect of steroids on the renovascular changes of sepsis. J Surg Res 1979, 26: 565-569. 10.1016/0022-4804(79)90051-9

    CAS  PubMed  Google Scholar 

  147. 147.

    Stone AM, Stein T, LaFortune J, Wise L: Changes in intrarenal blood flow during sepsis. Surg Gynecol Obstet 1979, 148: 731-734.

    CAS  PubMed  Google Scholar 

  148. 148.

    Tanigawa K, Bellomo R, Kellum JA, Kim YM, Zar H, Lancaster JR Jr, Pinsky MR, Ondulick B: Nitric oxide metabolism in canine sepsis: relation to regional blood flow. J Crit Care 1999, 14: 186-190. 10.1016/S0883-9441(99)90033-3

    CAS  PubMed  Google Scholar 

  149. 149.

    Tempel GE, Cook JA, Wise WC, Halushka PV: The improvement in endotoxin-induced redistribution of organ blood flow by inhibition of thromboxane and prostaglandin synthesis. Adv Shock Res 1982, 7: 209-218.

    CAS  PubMed  Google Scholar 

  150. 150.

    Tempel GE, Cook JA, Wise WC, Halushka PV, Corral D: Improvement in organ blood flow by inhibition of thromboxane synthetase during experimental endotoxic shock in the rat. J Cardiovasc Pharmacol 1986, 8: 514-519.

    CAS  PubMed  Google Scholar 

  151. 151.

    Tindel MS, Stone AM, Stein TA, Wise L: Effect of steroids on the cardiac output and renal changes of bacteremia. Am Surg 1985, 51: 716-720.

    CAS  PubMed  Google Scholar 

  152. 152.

    Townsend MC, Hampton WW, Haybron DM, Schirmer WJ, Fry DE: Effective organ blood flow and bioenergy status in murine peritonitis. Surgery 1986, 100: 205-213.

    CAS  PubMed  Google Scholar 

  153. 153.

    Treggiari MM, Romand JA, Burgener D, Suter PM, Aneman A: Effect of increasing norepinephrine dosage on regional blood flow in a porcine model of endotoxin shock. Crit Care Med 2002, 30: 1334-1339. 10.1097/00003246-200206000-00032

    CAS  PubMed  Google Scholar 

  154. 154.

    van Lambalgen AA, Runge HC, van den Bos GC, Thijs LG: Regional lactate production in early canine endotoxin shock. Am J Physiol 1988, 254: E45-E51.

    CAS  PubMed  Google Scholar 

  155. 155.

    van Lambalgen AA, van Kraats AA, van den Bos GC, Stel HV, Straub J, Donker AJ, Thijs LG: Renal function and metabolism during endotoxemia in rats: role of hypoperfusion. Circ Shock 1991, 35: 164-173.

    CAS  PubMed  Google Scholar 

  156. 156.

    van Lambalgen AA, van Kraats AA, van den Bos GC, Teerlink T, Stel HV, Donker AJ, Thijs LG: Development of renal failure in endotoxemic rats: can it be explained by early changes in renal energy metabolism? Nephron 1993, 65: 88-94.

    CAS  PubMed  Google Scholar 

  157. 157.

    van Lambalgen AA, van Kraats AA, Mulder MF, van den Bos GC, Teerlink T, Thijs LG: Organ blood flow and distribution of cardiac output in dopexamine- or dobutamine-treated endotoxemic rats. J Crit Care 1993, 8: 117-127. 10.1016/0883-9441(93)90016-E

    CAS  PubMed  Google Scholar 

  158. 158.

    Wanecek M, Rudehill A, Hemsen A, Lundberg JM, Weitzberg E: The endothelin receptor antagonist, bosentan, in combination with the cyclooxygenase inhibitor, diclofenac, counteracts pulmonary hypertension in porcine endotoxin shock. Crit Care Med 1997, 25: 848-857. 10.1097/00003246-199705000-00022

    CAS  PubMed  Google Scholar 

  159. 159.

    Wang P, Zhou M, Rana MW, Ba ZF, Chaudry IH: Differential alterations in microvascular perfusion in various organs during early and late sepsis. Am J Physiol 1992, 263: G38-G43.

    CAS  PubMed  Google Scholar 

  160. 160.

    Wang W, Jittikanont S, Falk SA, Li P, Feng L, Gengaro PE, Poole BD, Bowler RP, Day BJ, Crapo JD, et al.: Interaction among nitric oxide, reactive oxygen species, and antioxidants during endotoxemia-related acute renal failure. Am J Physiol Renal Physiol 2003, 284: F532-F537.

    CAS  PubMed  Google Scholar 

  161. 161.

    Weber A, Schwieger IM, Poinsot O, Klohn M, Gaumann DM, Morel DR: Sequential changes in renal oxygen consumption and sodium transport during hyperdynamic sepsis in sheep. Am J Physiol 1992, 262: F965-F971.

    CAS  PubMed  Google Scholar 

  162. 162.

    Weber A, Schwieger IM, Poinsot O, Morel DR: Time course of systemic and renal plasma prostanoid concentrations and renal function in ovine hyperdynamic sepsis. Clin Sci (Lond) 1994, 86: 599-610.

    CAS  Google Scholar 

  163. 163.

    White FN, Gold EM, Vaughn DL: Renin-aldosterone system in endotoxin shock in the dog. Am J Physiol 1967, 212: 1195-1198.

    CAS  PubMed  Google Scholar 

  164. 164.

    Xu D, Qi L, Guillory D, Cruz N, Berg R, Deitch EA: Mechanisms of endotoxin-induced intestinal injury in a hyperdynamic model of sepsis. J Trauma 1993, 34: 676-682. discussion 682-683.

    CAS  PubMed  Google Scholar 

  165. 165.

    Yang S, Zhou M, Koo DJ, Chaudry IH, Wang P: Pentoxifylline prevents the transition from the hyperdynamic to hypodynamic response during sepsis. Am J Physiol 1999, 277: H1036-H1044.

    CAS  PubMed  Google Scholar 

  166. 166.

    Yang S, Cioffi WG, Bland KI, Chaudry IH, Wang P: Differential alterations in systemic and regional oxygen delivery and consumption during the early and late stages of sepsis. J Trauma 1999, 47: 706-712.

    CAS  PubMed  Google Scholar 

  167. 167.

    Yang S, Koo DJ, Chaudry IH, Wang P: The important role of the gut in initiating the hyperdynamic response during early sepsis. J Surg Res 2000, 89: 31-37. 10.1006/jsre.1999.5807

    CAS  PubMed  Google Scholar 

  168. 168.

    Yang S, Zhou M, Fowler DE, Wang P: Mechanisms of the beneficial effect of adrenomedullin and adrenomedullin-binding protein-1 in sepsis: down-regulation of proinflammatory cytokines. Crit Care Med 2002, 30: 2729-2735. 10.1097/00003246-200212000-00018

    CAS  PubMed  Google Scholar 

  169. 169.

    Yang S, Zhou M, Chaudry IH, Wang P: Novel approach to prevent the transition from the hyperdynamic phase to the hypodynamic phase of sepsis: role of adrenomedullin and adrenomedullin binding protein-1. Ann Surg 2002, 236: 625-633. 10.1097/00000658-200211000-00013

    PubMed Central  PubMed  Google Scholar 

  170. 170.

    Yang S, Chung CS, Ayala A, Chaudry IH, Wang P: Differential alterations in cardiovascular responses during the progression of polymicrobial sepsis in the mouse. Shock 2002, 17: 55-60. 10.1097/00024382-200201000-00010

    CAS  PubMed  Google Scholar 

  171. 171.

    Yao K, Ina Y, Nagashima K, Ohno T, Karasawa A: Effect of the selective adenosine A1-receptor antagonist KW-3902 on lipopolysaccharide-induced reductions in urine volume and renal blood flow in anesthetized dogs. Jpn J Pharmacol 2000, 84: 310-315. 10.1254/jjp.84.310

    CAS  PubMed  Google Scholar 

  172. 172.

    Young JS, Passmore JC: Hemodynamic and renal advantages of dual cyclooxygenase and leukotriene blockade during canine endotoxic shock. Circ Shock 1990, 32: 243-255.

    CAS  PubMed  Google Scholar 

  173. 173.

    Zellner JL, Cook JA, Reines HD, Smith EF 3rd, Kessler LD, Halushka PV: Effect of a LTD4 receptor antagonist in porcine septic shock. Eicosanoids 1991, 4: 169-175.

    CAS  PubMed  Google Scholar 

  174. 174.

    Zhang H, Spapen H, Manikis P, Rogiers P, Metz G, Buurman WA, Vincent JL: Tirilazad mesylate (U-74006F) inhibits effects of endotoxin in dogs. Am J Physiol 1995, 268: H1847-H1855.

    CAS  PubMed  Google Scholar 

  175. 175.

    Zhang H, Rogiers P, Friedman G, Preiser JC, Spapen H, Buurman WA, Vincent JL: Effects of nitric oxide donor SIN-1 on oxygen availability and regional blood flow during endotoxic shock. Arch Surg 1996, 131: 767-774.

    CAS  PubMed  Google Scholar 

  176. 176.

    Zhang H, Rogiers P, Smail N, Cabral A, Preiser JC, Peny MO, Vincent JL: Effects of nitric oxide on blood flow distribution and O2 extraction capabilities during endotoxic shock. J Appl Physiol 1997, 83: 1164-1173.

    CAS  PubMed  Google Scholar 

  177. 177.

    Zhang H, De Jongh R, De Backer D, Cherkaoui S, Vray B, Vincent JL: Effects of alpha – and beta -adrenergic stimulation on hepatosplanchnic perfusion and oxygen extraction in endotoxic shock. Crit Care Med 2001, 29: 581-588. 10.1097/00003246-200103000-00020

    CAS  PubMed  Google Scholar 

  178. 178.

    Zhang H, De Jongh R, Cherkaoui S, Shahram M, Vray B, Vincent JL: Effects of nucleoside transport inhibition on hepatosplanchnic perfusion, oxygen extraction capabilities, and TNF release during acute endotoxic shock. Shock 2001, 15: 378-385.

    CAS  PubMed  Google Scholar 

  179. 179.

    Sward K, Valsson F, Sellgren J, Ricksten SE: Bedside estimation of absolute renal blood flow and glomerular filtration rate in the intensive care unit. A validation of two independent methods. Intensive Care Med 2004, 30: 1776-1782.

    PubMed  Google Scholar 

  180. 180.

    Guyton AC: Textbook of Medical Physiology. 7th edition. WB Saunders Company; 1986:394-396. [AU: please indicate the title of the chapter you are citing, and the place of the publisher.]

    Google Scholar 

  181. 181.

    Gilbert RP: Mechanisms of the hemodynamic effects of endotoxin. Physiol Rev 1960, 40: 245-279.

    CAS  PubMed  Google Scholar 

  182. 182.

    Wichterman KA, Baue AE, Chaudry IH: Sepsis and septic shock–a review of laboratory models and a proposal. J Surg Res 1980, 29: 189-201. 10.1016/0022-4804(80)90037-2

    CAS  PubMed  Google Scholar 

  183. 183.

    Parker MM, Shelhamer JH, Natanson C, Alling DW, Parrillo JE: Serial cardiovascular variables in survivors and nonsurvivors of human septic shock: heart rate as an early predictor of prognosis. Crit Care Med 1987, 15: 923-929.

    CAS  PubMed  Google Scholar 

  184. 184.

    Thijs A, Thijs LG: Pathogenesis of renal failure in sepsis. Kidney Int Suppl 1998, 66: S34-S37.

    CAS  PubMed  Google Scholar 

  185. 185.

    Winslow EJ, Loeb HS, Rahimtoola SH, Kamath S, Gunnar RM: Hemodynamic studies and results of therapy in 50 patients with bacteremic shock. Am J Med 1973, 54: 421-432. 10.1016/0002-9343(73)90038-7

    CAS  PubMed  Google Scholar 

  186. 186.

    Villazon SA, Sierra UA, Lopez SF, Rolando MA: Hemodynamic patterns in shock and critically ill patients. Crit Care Med 1975, 3: 215-221.

    CAS  PubMed  Google Scholar 

  187. 187.

    Mathiak G, Szewczyk D, Abdullah F, Ovadia P, Feuerstein G, Rabinovici R: An improved clinically relevant sepsis model in the conscious rat. Crit Care Med 2000, 28: 1947-1952. 10.1097/00003246-200006000-00043

    CAS  PubMed  Google Scholar 

  188. 188.

    Koo DJ, Zhou M, Chaudry IH, Wang P: The role of adrenomedullin in producing differential hemodynamic responses during sepsis. J Surg Res 2001, 95: 207-218. 10.1006/jsre.2000.6013

    CAS  PubMed  Google Scholar 

  189. 189.

    Wang P, Chaudry IH: Mechanism of hepatocellular dysfunction during hyperdynamic sepsis. Am J Physiol 1996, 270: R927-R938.

    CAS  PubMed  Google Scholar 

  190. 190.

    Di Giantomasso D, May CN, Bellomo R: Norepinephrine and vital organ blood flow. Intensive Care Med 2002, 28: 1804-1809. 10.1007/s00134-002-1444-x

    PubMed  Google Scholar 

Download references

Author information



Corresponding author

Correspondence to Rinaldo Bellomo.

Additional information

Competing interests

The author(s) declare that they have no competing interests.

Authors' contributions

CL conducted the searches and reviewed all necessary material, wrote the initial draft of the manuscript and performed statistical analysis. RB designed the study, critically reviewed the material and supervised the writing of the manuscript, CM co-designed the study and assisted with the completion of the manuscript. LW assisted with data assessment. ME assisted with data assessment and statistical analysis. SM assisted with study design and assessment, and completion of the manuscript.

Authors’ original submitted files for images

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Langenberg, C., Bellomo, R., May, C. et al. Renal blood flow in sepsis. Crit Care 9, R363 (2005).

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • DOI:


  • Cardiac Output
  • Acute Renal Failure
  • Renal Blood Flow
  • Renal Plasma Flow
  • Experimental Sepsis