Abstract
Our study evaluated the hypothesis that gastric contractions may contribute to ischemia by increasing vascular resistance. Using an ex vivo segment of the dog's stomach as the experimental model, contractions were induced with platelet activating factor (PAF) and bethanechol, a cholinergic vasodilator. Spontaneous contractions produced slight increases in luminal pressure and corresponding increases in vascular resistance. PAF caused statistically significant, dose-dependent increases in the force of gastric contractions that were highly correlated with phasic changes in vascular resistance. To ensure that the relationship between contractions and vascular resistance was independent of vascular tone, we next examined responses to bethanechol. Bethanechol stimulated contractions that also transiently increased both luminal pressure and vascular resistance. Our results demonstrate that gastric contractions markedly increase vascular resistance and support the hypothesis that hypercontractility may contribute to the development of mucosal ischemia during ulceration.
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