Masuda E, Kawano S, Nagano K, Ogihara T, Tsuji S, Tanimura H, Ishigami Y, Tsujii M, Hayashi N, Sasayama Y
Department of Medicine, Osaka University Medical School, Japan.
Alcohol Alcohol Suppl. 1991;1:335-8.
The present series of studies were performed to test the hypothesis that ethanol in the blood may play a role in the pathogenesis of gastric mucosal injury. Another hypothesis to be examined was that endothelin may be involved in ethanol-induced gastric mucosal injury. Elevated levels of blood ethanol induced by intraperitoneal infusion of ethanol increased vulnerability of the stomach to hydrochloric acid in a dose-dependent manner in rats. This may be due to impaired gastric mucosal hemodynamics and oxygenation as demonstrated by the results obtained by organ reflectance spectrophotometry (decreases in indices of mucosal hemoglobin contents and hemoglobin oxygen saturation). Ethanol infusion caused a dose-dependent increase in gastric vascular resistance in perfused rabbit stomach, which was accompanied by an increased production of endothelin-1. The results suggest that endothelin may be involved in the pathogenesis of ethanol-induced gastric mucosal injury.
开展本系列研究是为了验证血液中的乙醇可能在胃黏膜损伤发病机制中起作用这一假说。另一个有待检验的假说是内皮素可能参与乙醇诱导的胃黏膜损伤。腹腔注射乙醇导致血液中乙醇水平升高，使大鼠胃对盐酸的易损性呈剂量依赖性增加。这可能是由于胃黏膜血流动力学和氧合受损所致，器官反射分光光度法的结果表明（黏膜血红蛋白含量和血红蛋白氧饱和度指数降低）。乙醇灌注导致灌注兔胃的胃血管阻力呈剂量依赖性增加，同时伴有内皮素 -1 生成增加。结果表明内皮素可能参与乙醇诱导的胃黏膜损伤的发病机制。
