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一氧化氮合酶的抑制会延迟慢性胃溃疡的愈合。

Inhibition of nitric oxide synthase delays healing of chronic gastric ulcers.

作者信息

Konturek S J, Brzozowski T, Majka J, Pytko-Polonczyk J, Stachura J

机构信息

Institute of Physiology, University School of Medicine, Krakow, Poland.

出版信息

Eur J Pharmacol. 1993 Aug 3;239(1-3):215-7. doi: 10.1016/0014-2999(93)90997-v.

Abstract

We investigated the influence of inhibition of nitric oxide (NO) synthase, using NG-nitro-L-arginine (L-NNA) or NG-mono-methyl-L-arginine (L-NMMA), and the effects of exogenous donor of NO, such as glyceryl trinitrate (GTN), on the healing of chronic gastric ulcers induced by acetic acid, on gastric blood flow around the ulcer and on the number of capillaries in the granulation tissue at the ulcer bed. The inhibition of NO synthase resulted in a delay in ulcer healing and in a reduction in blood flow at the ulcer margin and in the number of capillaries in the granulation tissue at the ulcer bed. These effects of inhibition of NO synthase were antagonized, in part, by the administration of GTN or L-arginine but not D-arginine. We conclude that endogenous NO plays an important role in the maintenance of blood flow around the ulcer, in the angiogenesis in the granulation tissue and, thus, in the healing of gastric ulcers.

摘要

我们研究了使用 NG-硝基-L-精氨酸(L-NNA)或 NG-单甲基-L-精氨酸(L-NMMA)抑制一氧化氮(NO)合酶的影响,以及外源性 NO 供体如硝酸甘油(GTN)对醋酸诱导的慢性胃溃疡愈合、溃疡周围胃血流量和溃疡床肉芽组织中毛细血管数量的影响。抑制 NO 合酶导致溃疡愈合延迟,溃疡边缘血流量减少以及溃疡床肉芽组织中毛细血管数量减少。给予 GTN 或 L-精氨酸可部分拮抗抑制 NO 合酶的这些作用,但 D-精氨酸则无此作用。我们得出结论,内源性 NO 在维持溃疡周围血流、肉芽组织血管生成以及胃溃疡愈合过程中起着重要作用。

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