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J Appl Physiol (August 15, 2003). doi:10.1152/japplphysiol.00925.2002
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Submitted on October 10, 2002
Accepted on July 2, 2003

Gut Mucosal Damage during Endotoxic Shock is due to Mechanisms other than Gut Ischemia

Suzana M Lobo1, Daniel De Backer2, Qinghua Sun2, Zizhi Tu2, George Dimopoulos2, Jean-Charles Preiser2, Nathalie Nagy2, Bernard Vray2, Vincent Vercruy2, Renato G Terzi1, and Jean-Louis Vincent2*

1 Department of Emergency Medicine, Sao Paulo University Hospital, Sao Paulo, Brazil
2 Department of Intensive Care, Erasme University Hospital, Brussels, Belgium

* To whom correspondence should be addressed. E-mail: jlvincen{at}ulb.ac.be.

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 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, E. coli-055:B5, 150 µg/kg)/fluid resuscitation (12 ml/kg/h) (n=8); Group III, high dose LPS (1mg/kg)/fluid resuscitation (12 ml/kg/h) (n=8); Group IV, high dose LPS (1 mg/kg)/hypovolemia (4 ml/kg/h fluids) (n=8); and Group V, SMA ligation/fluid resuscitation (12 ml/kg/h) (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".




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