促胰液素对完全分离、血管灌注大鼠胃胃酸分泌作用的双重抑制机制

Dual inhibitory mechanism of secretin action on acid secretion in totally isolated, vascularly perfused rat stomach.

作者信息

Chung I, Li P, Lee K, Chang T, Chey W Y

机构信息

Department of Medicine, University of Rochester Medical Center, New York.

出版信息

Gastroenterology. 1994 Dec;107(6):1751-8. doi: 10.1016/0016-5085(94)90817-6.

DOI:10.1016/0016-5085(94)90817-6

PMID:7958688

Abstract

BACKGROUND/AIMS: Secretin is an inhibitory hormone of gastric acid secretion. However, its inhibitory mechanism has not been well understood. Possible roles of both somatostatin and prostaglandins were investigated.

METHODS

Totally isolated rat stomachs were vascularly perfused with Krebs-Ringer buffer containing 50 mumol/L isobutyl methylxanthine at 1.4 mL.min-1. Gastric lumen was perfused with 0.15 mol/L NaCl at 1.0 min.min-1. Effect of secretin in three different doses given intra-arterially on basal acid secretion and acid secretion stimulated by pentagastrin was studied. To determine roles of somatostatin and prostaglandins in the secretin-induced inhibition, an antisomatostatin serum and indomethacin were tested, and both somatostatin and prostaglandin E2 concentrations in portal venous effluent were determined by radioimmunoassay.

RESULTS

Both basal- and pentagastrin-stimulated acid secretion were significantly inhibited by secretin. The inhibition was completely reversed by either indomethacin or antisomatostatin serum. Secretin significantly increased concentrations of both somatostatin and prostaglandin E2. Although indomethacin blocked the increase in prostaglandin E2, secretin-induced increase in prostaglandin E2 was not affected by antisomatostatin serum or was indomethacin influenced by somatostatin level. Finally, the inhibition by somatostatin of acid secretion was not affected by indomethacin.

CONCLUSIONS

The inhibition of gastric acid secretion by secretin in rats is mediated by simultaneous releases of both somatostatin and prostaglandin E2, which independently inhibit gastric acid secretion.

摘要

背景/目的：促胰液素是一种胃酸分泌的抑制性激素。然而，其抑制机制尚未完全明确。本研究对生长抑素和前列腺素的可能作用进行了调查。

方法

将完全分离的大鼠胃用含50 μmol/L异丁基甲基黄嘌呤的 Krebs-Ringer 缓冲液以1.4 mL·min⁻¹的速度进行血管灌注。胃腔用0.15 mol/L氯化钠以1.0 mL·min⁻¹的速度进行灌注。研究了动脉内给予三种不同剂量促胰液素对基础胃酸分泌和五肽胃泌素刺激的胃酸分泌的影响。为了确定生长抑素和前列腺素在促胰液素诱导的抑制中的作用，检测了抗生长抑素血清和吲哚美辛，并通过放射免疫测定法测定了门静脉流出液中生长抑素和前列腺素E2的浓度。

结果

促胰液素显著抑制基础胃酸分泌和五肽胃泌素刺激的胃酸分泌。吲哚美辛或抗生长抑素血清均可完全逆转这种抑制作用。促胰液素显著增加了生长抑素和前列腺素E2的浓度。尽管吲哚美辛阻断了前列腺素E2的增加，但促胰液素诱导的前列腺素E2增加不受抗生长抑素血清的影响，或吲哚美辛不受生长抑素水平的影响。最后，生长抑素对胃酸分泌的抑制作用不受吲哚美辛的影响。