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Critical Care

Open Access

Renal arterial and microcirculatory blood flow during administration of Ornithin-8-Vasopressin in septic shock

  • L Hiltebrand1,
  • V Krejci1,
  • M Ten Hoevel1 and
  • GH Sigurdsson2
Critical Care20037(Suppl 2):P049

Published: 3 March 2003


PeritonitisRenal ArteryVasopressinGroup VersusRenal Cortex

Background and goal of study

The use of vasopressin for treatment of hypotension in sepsis might deteriorate splanchnic regional and microcirculatory blood flow. The aim of this study was to measure renal artery blood flow and microcirculatory blood flow (MBF) of the kidney continuously and simultaneously during administration of Ornithin-8-Vasopressin in peritonitis-induced sepsis.

Materials and methods

Pigs (20–25 kg, n = 32) were anaesthetised and ventilated. Cardiac index was measured with thermodilution. Blood flow was measured in the renal artery using transit time flowmetry. MBF was measured on the surface of the kidney using a multichannel Laser Doppler flowmeter. Peritonitis was induced by instillation of autologous faeces in the peritoneal cavity. After 240 min of peritonitis, intravenous colloids were given to transform hypodynamic shock into hyperdynamic septic shock. After 300 min of peritonitis, 0.06 IU/kg per hour of Ornithin-8-Vasopressin was administered continuously as an intravenous infusion. Four groups of animals were investigated: Group C (n = 8) served as control; Group V (n = 8) received only vasopressin; Group S (n = 8) was exposed to peritonitis and fluid resuscitation; Group SV (n = 8) received vasopressin after peritonitis and fluid resuscitation.

Results and discussion

Baseline measurements were taken at T = 300 min (before ornithin-vasopressin). Results are presented as percent of baseline. P < 0.05 was considered significant. Mean arterial blood pressure increased during infusion of vasopressin by 25% (P < 0.05) in groups V and SV (P > 0.05), while it remained constant in the other two groups. Cardiac output decreased by 30% in groups V and SV (P < 0.05) and remained constant in groups C and V. Renal artery blood flow decreased after 60 min of vasopressin by 15% (P < 0.05) in group V and returned to baseline after 180 min. In group SV, renal blood flow decreased by about 10% (P > 0.05) after 30 min and returned to baseline after 90 min. MBF of the kidney remained constant in groups C and S. In group V, MBF of the kidney decreased by 25% (P < 0.05) after 60 min of ornithin-vasopressin but returned to baseline after 180 min. In group SV, MBF of the kidney decreased by 15% (P < 0.05) and remained decreased. Urine output increased significantly in both septic and nonseptic groups receiving ornithin-vasopressin.

Discussion and conclusions

1) In nonseptic animals, blood flow in the renal artery and microcirculatory blood flow of the renal cortex decreased only initially and recovered after 180 min during infusion of vasopressin. This finding suggests the presence of an autoregulatory mechanism. 2) Although vasopressin decreased renal artery blood flow to a lesser extent in the septic group, microcirculatory blood flow decreased. This finding suggests that autoregulation at the microcirculatory level of the renal cortex might be impaired in sepsis. 3) In this model, increased urine output was not due to increased blood flow but rather the result of pressure diuresis.

Authors’ Affiliations

Department of Anaesthesiology and Intensive Care, University Hospital, Inselspital, Bern, Switzerland
Department of Anesthesia & Intensive Care Medicine, Landspitali University Hospital, Reykjavik, Iceland


© BioMed Central Ltd 2003