Abstract
The pathogenesis of ethanol-induced gastric mucosal damage in the rat is not fully understood. The effect of ethanol on the gastric submucosal microvessels and the possible role of arachidonic acid metabolites were studied. Intragastric administration of 5ml of 30% ethanol for 3min caused mucosal lesion of 32.6 ± 2.2% of the glandular stomach, which was attributed to congestion and cessation of mucosal capillary blood flow spreading from the collecting venule. This lesion was inhibited to 18.0±3.6% by pretreatment of AA-861 (80 mg/kg, p.o.) . The immunoreactive-leukotriene C4 (i-LTC4) content in the gastric wall was 0.6±0.1 ng/stomac in the resting state, and was significantly increased to 4.0±0. 5 ng/stomach after 30% ethanol in the gastric lumen. Intragastric administration of 1.0 M NaCl caused increase in PGE2 levels in the gastric lumen. The electrical activity of the gastric smooth muscle was also suppressed by 1.0 M NaCl solution.
It may be concluded that endogenous i-LTC4 generated in the gastric wall after 30% ethanol constricts the collecting venule and induces the congestion of the mucosal blood flow and the lesion suppresses by increased PGE2 for suppressed smooth muscle contraction.
