作者: Bashir O Attuwaybi , Heitham T Hassoun , Lei Zou , Rosemary A Kozar , Bruce C Kone
DOI: 10.1016/S0022-4804(03)00313-5
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摘要: Abstract Purpose. Gut ischemia/reperfusion (I/R) elicits an inflammatory response that impairs intestinal transit. We have previously shown regional intraischemic hypothermia (IH) protects against moderate gut I/R-induced mucosal injury, is associated with decreased NF-κB activity and inducible nitric oxide synthase induction preserves heme oxygenase-1 (HO-1) expression. HO-1 provides cytoprotection in various models of oxidant stress. We, therefore, tested the hypothesis IH impaired transit via induction. Materials methods. At laparotomy (lap), Sprague—Dawley rats had duodenal catheters placed followed by sham or I/R (superior mesenteric artery occlusion for 75 min) without (15°C). Each animal was on a heating blanket maintaining systemic normothermia (37°C). 12 24 h reperfusion, small determined quantitating distribution tracer (FITC dextran) intestine 30 min after instillation (expressed as geometric center distribution). Ileal samples were obtained histology expression, assessed Western immunoblot at reperfusion. In separate experiments, pretreated inhibitor Sn protoporphyrin IX (25 μmol/kg, ip), 1 before superior measured above. Results. Rats treated increased histological injury both compared sham. I/R+IH exhibited comparable controls. induced expression reperfusion augmented this abrogated protection Conclusion. conclude caused severe injury. Hypothermic under these conditions part due to