Mechanism of gastric mucosal lesion formation in portal hypertension with special reference to microcirculation and vasoactive substances

Whether vasoactive substances including cathecholamines, serotonin, endothelin (ET), glucagon and nitric oxide (NO) are involved in the gastric microcirculatory changes such as constriction of submucosal arterioles in acute portal hypertension was studied in rats. Portal vein pressure mas increased stepwisely by the partial ligation of the portal vein. Blood levels of the vasoactive substances in the portal vein mere measured, and an in vitro microscopy was used to observe the gastric submucosal vessels. There were no significant differences of the blood level of epinephrine, norepinephrine, dopamine, serotonin, and total and pancreatic glucagons only with significant difference of endothelin between the control and portal hypertension groups. BQ-123Na, ET-receptor subtype antagonist, inhibited the constriction of. the arterioles dose-dependently, and dilated the arterioles (10(-6) M). L-MMA, inhibitor of NO synthesis, inhibited the dilatation. These results suggested both ET and NO are involved in the gastric microcirculatory changes and the submucosal arterioles are constricted through the predominant function of ET in acute portal hypertension.