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Influence of bacterial translocation in the genesis of the microcirculation: hypoperfusion in sepsis
Critical Carevolume 11, Article number: P24 (2007)
Increasing evidence suggests that bacterial translocation (BT) has been implicated in the pathogenesis of sepsis and multiple organ failure. In this study we examined the role of the mesenteric lymph during the BT process on the intestinal and systemic tissue perfusion in association with nonlethal sepsis.
Materials and methods
Adult Wistar rats (± 200 g) were submitted to the induction of BT (E. coli R6 10 ml of 1010 CFU/ml), sepsis (E. cloacae 89 2 ml of 107 CFU/ml, i.v.) and sepsis plus BT, with or without interruption of the mesenteric lymph flow by mesenteric lymph node resection and lymph duct ligature 5 days prior to the experiments. The tissue perfusion (jejunum, ileum, liver and kidneys) was monitored (laser Doppler) before and 2 hours after the inoculation. Groups (n = 16/group): BT group (BT-G); BT with lymphadenectomy group (BTL-G); sepsis group (S-G); sepsis with lymphadenectomy group (SL-G); combination of sepsis plus BT group (C-G); combination with lymphadenectomy group (CL-G); sham BT group (SBT-G); sham sepsis group (SS-G); and sham combination group (SC-G).
Following BT induction, with or without sepsis or lymphadenectomy, the bacterial recovery was 100% in all groups. A significant and similar reduction of the tissue perfusion was observed in all organs in BT-G (P < 0.0001) and C-G (P < 0.0001). However, with lymph interruption (BTL-G and CL-G), the tissue perfusion drop was completely abrogated and was as similar as the respective sham groups (Figure 1). Mortality of 50% (LD50) was observed only in C-G.
The components of the mesenteric lymph during the BT process were a determinant factor related to the impairment of the splachnic and systemic tissue perfusion index possibly by gut-associated tissue activation, suggesting a possible participation of BT in the genesis of the hypodynamic state of sepsis.