Ward A S, Bloom S R
Gut. 1974 Nov;15(11):889-97. doi: 10.1136/gut.15.11.889.
The effect of intraduodenal acid on pentagastrin-stimulated gastric secretion has been investigated in 12 normal subjects and 23 patients with chronic duodenal ulceration. Plasma secretin levels were monitored during each test using a highly sensitive radioimmunoassay. Significant inhibition of gastric secretion occurred in the normal subjects and duodenal ulcer patients. A significant rise in plasma secretin was observed in both groups after intraduodenal acid though there was a complete lack of correlation between the magnitude of the secretin response and the degree of gastric inhibition. Ten subjects received intraduodenal acid and a subsequent intravenous infusion of exogenous secretin (0.125-0.25 units/kg over six minutes). Gastric inhibition occurred after the acid instillation but not after secretin infusion despite plasma secretin levels greatly in excess of those produced by intraduodenal acid. These results suggest that release of secretin by itself cannot explain the gastric inhibitory response to intraduodenal acid in man.
在12名正常受试者和23名慢性十二指肠溃疡患者中,研究了十二指肠内酸对五肽胃泌素刺激的胃分泌的影响。在每次试验期间,使用高灵敏度放射免疫分析法监测血浆促胰液素水平。正常受试者和十二指肠溃疡患者的胃分泌均受到显著抑制。十二指肠内注入酸后,两组受试者的血浆促胰液素均显著升高,尽管促胰液素反应的幅度与胃抑制程度之间完全缺乏相关性。10名受试者接受十二指肠内酸注入,随后静脉输注外源性促胰液素(6分钟内0.125 - 0.25单位/千克)。注入酸后出现胃抑制,但促胰液素输注后未出现胃抑制,尽管血浆促胰液素水平大大超过十二指肠内酸产生的水平。这些结果表明,促胰液素自身的释放不能解释人体对十二指肠内酸的胃抑制反应。