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大鼠胃黏膜的黏液分泌与细胞保护作用

Mucosal secretion and cytoprotection of the rat gastric mucosa.

作者信息

Morris G P, Basu B K, Holitzner C A, Williamson T E

机构信息

Gastrointestinal Diseases Research Unit, Queen's University, Kingston, Ontario, Canada.

出版信息

J Clin Gastroenterol. 1993;17 Suppl 1:S5-10. doi: 10.1097/00004836-199312001-00004.

Abstract

We carried out a series of experiments to test the hypothesis that many examples of gastric cytoprotection result from the ability of protective agents to elevate mucosal secretion. Specifically, such protection would be effective against barrier breakers that act directly on the mucosal surface. We have previously observed that the protection found to result, in our rat gastric chamber model, from luminal stasis or from sucralfate, was accompanied by increases in the thickness of a juxtamucosal pH gradient. The pH gradient was measured with antimony microelectrodes and was about 900 microns thick over chambered gastric mucosae that had not had the luminal solution stirred for at least 5 min. When the solution was stirred (200 rpm) for 10 min with a plastic paddle, the thickness of the pH gradient was decreased to about 400 microns but recovered to more than 90% of the starting value within 5 min. The thickness of the pH gradient varied from site to site, with a range from about 500 microns to 1,800 microns. However, the thickness was constant at a given site when it was remeasured after about 1 h. Capsaicin at a concentration of 640 microM rapidly increased both gastric blood flow and the thickness of the juxtamucosal pH gradient by about 50%. However, 25 min after removal of the capsaicin the gastric blood flow approached pre-capsaicin levels, and the thickness of the gradient remained increased by nearly 50%. In a third set of experiments, the vulnerability of specific sites on the chambered mucosae to acidified sodium taurocholate was correlated with the thickness of the juxtamucosal pH gradient before exposure to taurocholate.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们进行了一系列实验,以检验以下假设:许多胃细胞保护的例子是由于保护剂提高粘膜分泌的能力所致。具体而言,这种保护对直接作用于粘膜表面的屏障破坏剂有效。我们之前观察到,在我们的大鼠胃腔模型中,由管腔淤滞或硫糖铝产生的保护作用伴随着近粘膜pH梯度厚度的增加。pH梯度用锑微电极测量,在至少5分钟未搅拌管腔溶液的有腔胃粘膜上,其厚度约为900微米。当用塑料桨以200转/分钟搅拌溶液10分钟时,pH梯度厚度降至约400微米,但在5分钟内恢复到起始值的90%以上。pH梯度厚度因部位而异,范围约为500微米至1800微米。然而,在约1小时后重新测量时,给定部位的厚度是恒定的。浓度为640微摩尔的辣椒素使胃血流量和近粘膜pH梯度厚度迅速增加约50%。然而,去除辣椒素25分钟后,胃血流量接近辣椒素处理前的水平,梯度厚度仍增加近50%。在第三组实验中,有腔粘膜上特定部位对酸化牛磺胆酸钠的敏感性与暴露于牛磺胆酸钠之前近粘膜pH梯度的厚度相关。(摘要截短于250字)

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