EXPERIMENTAL STUDIES ON DEVELOPMENTAL MECHANISM OF ACUTE HEMORRHAGIC GASTRIC ULCERS WITH EMPHASIS ON THE EFFECTS OF HISTAMINE

Studies to elucidate the mechanism responsible for histamine effects on the development of acute hemorrhagic ulcers were undertaken using laboratory animals, i. e. a control group consisting of rats with chronic gastric fistula, V. B6 deficient diet group, cimetidine administered group and vagotomized group. The respective groups were subjected to cold restraint and the degree of hemorrhage, erosion, gastric acid secretion, gastric mucosal histamine content and state of microvasculature of gastric mucosa were observed over time, and the following results were obtained.
1. There was a decrease in the degree of hemorrhage and erosion in the V. B6 deficient diet and cimetidine administered groups and the vagotomized group.
2. Gastric acid secretion was significantly decreased in all groups subjected to cold restraint for up to 60 minutes.
3. The gastric mucosal histamine content was significantly decreased in the control and cimetidine administered groups after cold restraint for 30 minutes. In the V. B6 deficient diet group, the content decreased to about 1/3, but failed to demonstrate a significant difference. The vagotomized group showed a two-fold increase, which after cold restraint for 120 minutes decreased significantly.
4. The microvasculature of the gastric mucosa in the control group was. poorly visualized by FITC-dextran method and presented a static appearance. In the other three groups, the capillaries of the gastric mucosa were well visualized and no static pattern was observed.

The above findings suggest that histamine in the gastric mucosa is released by cold restraint and acts upon microcirculation within the gastric mucosa rather than upon gastric acid secretion, causing stasis and mucosal devitalization, and thus assumes a role in the development of ulcer.