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Gut mucosal damage during endotoxic shock is due to mechanisms other than gut ischemia

¹Department of Intensive Care, Faculdade de Medicina de Sao José do Rio Preto, 15091-450 Sao José; and ³Emergency Department, University of Sao Paulo, 05508-010 Sao Paulo, Brazil; and ²Department of Intensive Care, Erasme Hospital, Free University of Brussels, 1070 Brussels, Belgium

Submitted 10 October 2002 ; accepted in final form 2 July 2003

Whether the gut alterations seen during sepsis are caused by microcirculatory hypoxia or disturbances in cellular metabolic pathways associated with mitochondrial respiration remains controversial. We hypothesized that hypoperfusion or hypoxia and local production of nitric oxide might play an important role in the development of gut mucosal injury during endotoxic shock and investigated their roles by using differing levels of fluid resuscitation and occlusion of the superior mesenteric artery (SMA). Anesthetized New Zealand rabbits were allocated to group I (sham, n = 8); group II [low-dose endotoxin (LPS, Escherichia coli-055:B5, 150 µg/kg)/fluid resuscitation (12 ml · kg^-1 · h^-1); n = 8]; group III [high-dose LPS (1 mg/kg)/fluid resuscitation (12 ml · kg^-1 · h^-1); n = 8]; group IV [high-dose LPS (1 mg/kg)/hypovolemia (4 ml · kg^-1 · h^-1 fluids); n = 8]; and group V [SMA ligation/fluid resuscitation (12 ml · kg^-1 · h^-1); n = 4]. Luminal gut lactate concentrations and PCO₂ gap increased in groups IV and V (P < 0.05), reflecting alterations in gut perfusion. Interestingly, significant histological alterations were observed in all LPS groups but not in group V. Blood and luminal gut nitrate/nitrite concentrations increased only in group IV. The mechanism of gut injury in endotoxic shock seems unrelated to hypoxia and release of nitric oxide. Gut dysfunction may occur as a result of so-called "cytopathic hypoxia."

sepsis; lactate; nitric oxide; cytopathic hypoxia

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