[A study on the mechanism of development of acute gastric ulcer in hemorrhagic shock--with special reference to the relation of PGE2 and noradrenaline levels in the gastric mucosa and changes in gastric mucosal blood flow].

Changes in gastric mucosal blood flow in acute gastric ulceration associated with hemorrhagic shock were investigated for their relationship to gastric mucosal PGE2 and NA in rats which were deprived of 24 ml/kg of blood. The results were: 1. Gastric mucosal blood flow and NA were decreased by 65% and 25% respectively at 30 minutes after hemorrhage. Gastric mucosal PGE2 was 26% increased at 30 minutes after exsanguination and then showed a marked decrease. 2. Administration of NA resulted in an 100% increase of gastric mucosal PGE2. However, animals receiving NA at 20 or 50 minutes after hemorrhage gave values for gastric mucosal PGE2 which were not different from those of non-NA-treated animals at 30 and 60 minutes after hemorrhage. 3. Pre-treatment with PGE2 suppressed the reduction in both gastric mucosal blood flow and NA and the development of ulcer, whereas pre-treatment with indomethacin accelerated them. These results suggest that the increase in gastric mucosal PGE2 in early shock might represent a phenomenon of adaptation to decreased blood flow, implicating adrenergic activation as one of causative factors, and the decrease in gastric mucosal PGE2 in late shock might be construed as the result of impaired synthesis of PGE2 due to persistent hypoxia and be one of the possible factors for ulcers.