Development of ischemia/reperfusion tolerance in the rat small intestine. An epithelium-independent event.

Abstract

In stable organ systems, such as the heart and kidneys, an oxidant stress induces an increase in endogenous antioxidant systems resulting in an increased resistance of the tissue to a subsequent oxidant challenge. The development of this oxidant tolerance requires 1.5-6 d. The aim of the present study was to determine whether oxidant tolerance can be induced in the small intestinal mucosa, a labile system whose epithelium turns over every 2-3 d. Ischemia/reperfusioninduced epithelial barrier dysfunction of the small intestinal mucosa was monitored in Sprague-Dawley rats whose intestines had been exposed to an ischemic insult 1, 24, or 72 h previously. At 24 h, but not 1 or 72 h after the initial ischemic insult, the mucosa was more resistant to ischemia/ reperfusion-induced barrier dysfunction. The antioxidant status of the mucosa was enhanced at 24 h, but not at 1 or 72 h after the initial ischemic insult. This adaptation appears to be specific for oxidants, since an initial ischemic insult imposed 24 h earlier also protected against H202-induced, but not acid-or ethanol-induced, barrier dysfunction. Further studies indicated that the increase in antioxidant status of the mucosa observed 24 h after the initial ischemic insult was a result of adaptational changes in the lamina propria, rather than the epithelium. In vitro studies with isolated epithelial cells also indicated that epithelial cells do not develop oxidant tolerance. We conclude that the development of oxidant tolerance in the small intestinal mucosa does not involve an active participation of the epithelial lining. (J.

Effect of Some Natural Products Either Alone or in Combination on Gastritis Induced in Experimental Rats

“…However, severe oxidative stress can decrease tissue antioxidant levels [40]. Such an adaptation effect had been observed in previous studies including the small intestinal, gastric, and duodenal mucosa [41,42].…”

Vascular Pathology of Ischemia/Reperfusion Injury of Rat Small Intestine

“…However, endothelial dysfunction precedes the mucosal damage in the pathogenesis of I/R [Granger et al, 1980;Osborne et al, 1994.]. Based on these preconditions, in our study, we analyzed the correlation between the development of injury of the microcirculatory component and the intestinal tissue.…”

Anoxia/Reoxygenation-Induced Tolerance With Respect to Polymorphonuclear Leukocyte Adhesion to Cultured Endothelial Cells

“…This phenomenon, termed "I/R tolerance" has been demonstrated in the heart, 5,6 kidneys, 7 brain, 8 and intestine. 9 Typically, I/R tolerance requires several hours or days to develop, indicating that some transcriptional event may be involved. Studies in the intestine indicate that the development of I/R tolerance is not due to an adaptational response of the parenchymal cells but to some cell type in the lamina propria.…”

“…Studies in the intestine indicate that the development of I/R tolerance is not due to an adaptational response of the parenchymal cells but to some cell type in the lamina propria. 9 Endothelial cells are a resident cell population of the lamina propria of a variety of organ systems. They can also mount an adaptational response to an oxidant stress that renders them less susceptible to the injurious effects of a second oxidant challenge imposed several hours later.…”