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.