Ischemia-reperfusion increases gastric motility and endothelin-1-induced vasoconstriction.
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.
D000818:Animals; D004285:Dogs; D016232:Endothelins / Q000494:pharmacology*; D005769:Gastrointestinal Motility / Q000187:drug effects; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D015424:Reperfusion; D013270:Stomach / Q000098:blood supply*; D013482:Superoxide Dismutase / Q000494:pharmacology; D014661:Vasoconstriction
D016232:Endothelins; D013482:Superoxide Dismutase