Gastrin produces an immediate and dose-dependent histamine release preceding acid secretion in the totally isolated, vascularly perfused rat stomach.
Gastrin produces an immediate and dose-dependent histamine release preceding acid secretion in the totally isolated, vascularly perfused rat stomach.
复制标题
在完全隔离、血管灌注的大鼠胃中，胃泌素在酸分泌之前立即产生剂量依赖性组胺释放。
DOI：
10.3109/00365528708991918
复制
发表时间：
1987
影响因子：
1.9
通讯作者：
B. Søgnen
中科院分区：
文献类型：
--
作者：
A. Sandvik;H. Waldum;P. M. Kleveland;B. Søgnen
增加剂量的胃泌素1-17（G1-17）给予完全分离的，血管灌注的大鼠胃预刺激的磷酸二酯酶抑制剂异丁基甲基黄嘌呤（IMX）。以短时间间隔监测血管和管腔组胺输出和管腔酸输出。G1-17诱导组胺立即释放到血管灌注液中，在酸分泌增加之前约10分钟。血管组胺输出从基线增加（仅IMX）4.0 +/- 0.4至最大值34.5 +/- 7.3 nmol/60 min（平均值+/- SEM），520 pM G1 - 17后酸输出从8.0 +/- 2.8至61.5 +/- 7.0 mumol/60 min。酸输出量与血管组胺释放相关（r = 0.64，p <0.001）。胃泌素产生组胺释放，使胃静脉浓度与诱导可比较的酸反应所需的组胺浓度相同。另一方面，组胺释放到管腔，及时抑制酸分泌，表明它是继发于酸分泌的被动现象。因此，本研究首次表明，胃泌素诱导血管组胺释放的幅度，这种物质可能是介质的胃泌素对酸分泌的影响。
Increasing doses of gastrin 1-17 (G1-17) were administered to totally isolated, vascularly perfused rat stomachs prestimulated with the phosphodiesterase inhibitor isobutyl methylxanthine (IMX). Vascular and luminal histamine outputs and luminal acid output were monitored at short intervals. G1-17 induced an immediate histamine release to the vascular perfusate, preceding the increase in acid secretion by approximately 10 min. Vascular histamine output increased from a base line (IMX only) of 4.0 +/- 0.4 to a maximum of 34.5 +/- 7.3 nmol/60 min (mean +/- SEM) after 1040 pM G1-17, and acid output from 8.0 +/- 2.8 to 61.5 +/- 7.0 mumol/60 min after 520 pM G1-17. Acid output was correlated to vascular histamine release (r = 0.64, p less than 0.001). Gastrin produced a histamine release giving gastric venous concentrations of the same magnitude as the concentration of histamine necessary to induce a comparable acid response. Histamine release to the lumen, on the other hand, paralleled the acid secretion in time, suggesting it to be a passive phenomenon secondary to acid secretion. Thus, the present study for the first time shows that gastrin induces vascular histamine release of such a magnitude that this substance could be the mediator of the gastrin effect on acid secretion.