STUDIES ON SERUM GASTRIN RESPONSE TO INTRAVENOUS ADMINISTRATION OF ARGININE IN MAN

Abstract

Even less is known about the role of gastrin, the most potent stimulator of gastric acid secretion, in the pathogenesis of peptic ulcer disease. The present study was undertaken to determine arginine-stimulated gastrin release in patients with peptic ulcer.The results obtained herein were as follows : 1. The mean fasting serum gastrin concentrations for the patients with gastric ulcer and duodenal ulcer did not differ from that of normal subjects.2. Intravenous drip infusion of L-arginine (0.5g/kg, 30min) to normal subjects caused a significant rise in serum gastrin levels to approximately 130% of the baseline at 10min.3. The peak values of serum gastrin, insulin, growth hormone and glucagon following arginine infusion were achieved at 10, 30, 45 and 30min. respectively.4. The mean basal (BAO) and maximum gastric acid secretion (MAO) were greater in duodenal ulcer patients than in gastric ulcer patients. However, those of gastric ulcer patients were less than those of control subjects, although no significant differences between two groups were obtained.5. Arginine-induced gastrin release was significantly greater in duodenal ulcer patients than in gastric ulcer patients. There was no difference between gastric ulcer patients and normal subjects.6. According to the arginine-induced gastrin release, gastric ulcer patients were divided into 3groups : three types of high, normal and low gastrin response. High gastrin response group appeared to be related to the increased mucosal atrophy in the stomach, low gastric acid secretion and non-relapse cases of ulceration.7. In duodenal ulcer patients, gastrin response to arginine was neither associated with increased mucosal atrophy nor diminished gastric acid secretion.Thus, we have demonstrated that intravenous drip infusion of arginine is an effective stimulus for the release of gastrin. The observations described in this report have failed to support the concept that gastrin stasis is the cause of gastric ulcer. However, the increased susceptibility of gastrin release to arginine in duodenal ulcer patients suggests the potential importance of gastrin in the hypersecretory state that frequently characterizes duodenal ulcer disease.