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大鼠胃损伤后胃碱性反应中的内源性一氧化氮

Endogenous nitric oxide in gastric alkaline response in the rat stomach after damage.

作者信息

Takeuchi K, Ohuchi T, Okabe S

机构信息

Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.

出版信息

Gastroenterology. 1994 Feb;106(2):367-74. doi: 10.1016/0016-5085(94)90594-0.

DOI:10.1016/0016-5085(94)90594-0
PMID:8299903
Abstract

BACKGROUND/AIMS: The gastric mucosa responds to hypertonic NaCl by significantly decreasing acid secretion. This study examined the role of nitric oxide in this phenomenon.

METHODS

A rat stomach was mounted in an ex vivo chamber and perfused with saline; then the potential difference (PD), pH, and acid and/or alkaline responses were measured before and after the application of 1 mol/L NaCl with or without pretreatment with NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO biosynthesis.

RESULTS

A dose of 1 mol/L NaCl caused a reduction in PD, a decrease in basal and histamine-stimulated acid secretion, and an increase in luminal HCO3-. Prior administration of L-NAME did not affect either the PD or the HCO3- response but significantly attenuated the inhibitory effect of 1 mol/L NaCl on acid secretion. This effect of L-NAME was antagonized by the simultaneous administration with L-arginine but not D-arginine. Histamine-stimulated acid secretion in the normal stomach was significantly reduced by the exogenous NO donor nitroprusside but not by L-NAME.

CONCLUSIONS

NO is involved in the mechanism of the gastric alkaline response after damage with 1 mol/L NaCl. Irritation of the gastric mucosa by hypertonic NaCl may release endogenous NO, which in turn inhibits acid secretion and unmasks luminal alkalinization caused by HCO3- flux in the damaged portion.

摘要

背景/目的:胃黏膜对高渗氯化钠的反应是显著减少胃酸分泌。本研究探讨一氧化氮在这一现象中的作用。

方法

将大鼠胃置于离体腔室中,用生理盐水灌注;然后在应用1mol/L氯化钠之前和之后,测量电位差(PD)、pH值以及酸和/或碱反应,应用时或预先用一氧化氮生物合成抑制剂NG-硝基-L-精氨酸甲酯(L-NAME)预处理。

结果

1mol/L氯化钠剂量导致PD降低、基础和组胺刺激的胃酸分泌减少以及管腔碳酸氢根增加。预先给予L-NAME对PD或碳酸氢根反应均无影响,但显著减弱了1mol/L氯化钠对胃酸分泌的抑制作用。L-NAME的这种作用可被同时给予L-精氨酸拮抗,但不能被D-精氨酸拮抗。正常胃中组胺刺激的胃酸分泌可被外源性一氧化氮供体硝普钠显著降低,但不能被L-NAME降低。

结论

一氧化氮参与1mol/L氯化钠损伤后胃碱性反应的机制。高渗氯化钠对胃黏膜的刺激可能释放内源性一氧化氮,进而抑制胃酸分泌,并揭示受损部位由碳酸氢根通量引起的管腔碱化。

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