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Am J Physiol Gastrointest Liver Physiol 269: G524-G531, 1995;
0193-1857/95 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 269, Issue 4 524-G531, Copyright © 1995 by American Physiological Society

ARTICLES

Ischemia-reperfusion increases gastric motility and endothelin-1-induced vasoconstriction

J. G. Wood, Z. Y. Yan, Q. Zhang and L. Y. Cheung
Department of Surgery, University of Kansas Medical Center, Kansas City 66160, USA.

The purpose of our study was to 1) examine the effect of ischemia-reperfusion on gastric vascular resistance and motility, 2) determine whether endothelin-1 (ET-1)-induced vasoconstriction is enhanced after ischemia-reperfusion, and 3) assess the effect of superoxide dismutase (SOD) on these ischemia-reperfusion-induced alterations. These experiments used a mechanically perfused ex vivo gastric segment of chloralose-anesthetized dogs. We first evaluated the effect of varying the duration of total ischemia on reperfusion-induced changes in gastric vascular resistance and motility. In other experiments, responses to ET-1 (10(-10) M) were compared before and after 30-min ischemia and 30-min reperfusion, with saline or SOD (10 U/ml) infused intra-arterially to the stomach during reperfusion. Our results show that 1) after ischemia, vasodilation is seen initially on reperfusion followed by a slowly developing, progressive increase in vascular resistance, 2) the force of gastric contractions was reduced during ischemia but elevated immediately on reperfusion, 3) vasoconstrictor responses to ET-1 are enhanced after ischemia-reperfusion, and 4) SOD reduced the enhanced response to ET-1 and force of contractions. Our findings support the hypothesis that reactive oxygen metabolites contribute to augmented vascular reactivity and hypercontractility after ischemia-reperfusion.


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