Lucey M R, Wass J A, Rees L H, Dawson A M, Fairclough P D
Department of Gastroenterology, Saint Bartholomews Hospital, West Smithfield, London, United Kingdom.
Gastroenterology. 1989 Oct;97(4):867-72. doi: 10.1016/0016-5085(89)91490-x.
The aim of this study was to examine whether hydrochloric acid plays a role mediating the post-prandial increase in plasma somatostatinlike immunoreactivity in normal subjects. Intravenous infusion of cimetidine was found to reduce by 45% the postprandial increment in plasma somatostatin-like immunoreactivity. This effect was reversed by concomitant intragastric administration of 0.1 N hydrochloric acid, which in previous studies in fasted subjects had not affected plasma somatostatinlike immunoreactivity. The effects of cimetidine on postprandial plasma gastrin were the inverse of those observed on postprandial somatostatin. There was a greatly enhanced increment in postprandial plasma gastrin during cimetidine infusion, which was reduced significantly toward control levels by concomitant intragastric infusion of hydrochloric acid. To exclude direct inhibition by cimetidine of nutrient-stimulated plasma somatostatinlike immunoreactivity we studied the effect of cimetidine on plasma somatostatinlike immunoreactivity stimulated by an intraduodenal infusion of fat. Cimetidine did not alter the incremental response of somatostatinlike immunoreactivity to intraduodenal fat infusion. These data show that cimetidine does not invariably reduce nutrient-stimulated plasma somatostatinlike immunoreactivity and are consistent with the hypothesis that the action of cimetidine in reducing the plasma somatostatin response to ingestion of a meal is a consequence of reduction of postprandial acid secretion. These data suggest that the postprandial elevation in plasma somatostatin observed in humans is mediated in part through postprandial secretion of gastric acid, which in turn acts to elevate plasma somatostatin.
本研究的目的是检验盐酸在正常受试者餐后血浆生长抑素样免疫活性增加过程中是否起介导作用。结果发现，静脉输注西咪替丁可使餐后血浆生长抑素样免疫活性的增加降低45%。同时胃内给予0.1 N盐酸可逆转这一效应，而在先前对空腹受试者的研究中，该盐酸并未影响血浆生长抑素样免疫活性。西咪替丁对餐后血浆胃泌素的作用与对餐后生长抑素的作用相反。在输注西咪替丁期间，餐后血浆胃泌素的增加显著增强，而同时胃内输注盐酸可使其显著降低至对照水平。为排除西咪替丁对营养物质刺激的血浆生长抑素样免疫活性的直接抑制作用，我们研究了西咪替丁对十二指肠内输注脂肪刺激的血浆生长抑素样免疫活性的影响。西咪替丁并未改变生长抑素样免疫活性对十二指肠内输注脂肪的增量反应。这些数据表明，西咪替丁并非总是降低营养物质刺激的血浆生长抑素样免疫活性，这与以下假设一致，即西咪替丁降低血浆生长抑素对进餐反应的作用是餐后胃酸分泌减少的结果。这些数据提示，人类餐后血浆生长抑素的升高部分是由餐后胃酸分泌介导的，而胃酸分泌反过来又会使血浆生长抑素升高。
