NITRIC OXIDE-MEDIATED GASTRIC HYPEREMIA DECREASES ETHANOL-INDUCED GASTRIC-MUCOSAL INJURY IN UREMIC RATS

被引：19

作者：

QUINTERO, E

GUTH, PH

机构：

[1] UNIV CALIF LOS ANGELES,VET ADM MED CTR W LOS ANGELES,MED SERV,W111C,LOS ANGELES,CA 90073

[2] UNIV CALIF LOS ANGELES,VET ADM MED CTR W LOS ANGELES,RES SERV,LOS ANGELES,CA 90024

[3] CTR ULCER RES & EDUC,LOS ANGELES,CA

来源：

DIGESTIVE DISEASES AND SCIENCES | 1992年 / 37卷 / 09期

关键词：

GASTRIC MUCOSAL BLOOD FLOW; ENDOTHELIUM-DERIVED RELAXING FACTOR; CHRONIC RENAL FAILURE;

D O I：

10.1007/BF01295999

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

We investigated whether the recently described endothelium-derived nitric oxide-mediated gastric hyperemia in the uremic rat protects the gastric mucosa against ethanol injury. Uremia was induced by subtotal nephrectomy. Basal gastric mucosal blood flow, measured by a hydrogen gas clearance technique, was significantly higher in uremic than control rats. Continuous intragastric perfusion with 40% ethanol produced significantly less gross and histological lesions in uremic than in control rats. The administration of 3 mg/kg of N(W)-nitro-L-arginine methyl ester, a specific inhibitor of nitric oxide biosynthesis, decreased resting gastric mucosal blood flow to control levels in uremic rats, but had no effect on basal gastric blood flow in control rats. This pretreatment with the inhibitor of nitric oxide biosynthesis increased 40% ethanol-induced gastric mucosal lesions in uremic rats to the same level as that observed in control rats, but had no effect on lesions in control rats. In conclusion, this study suggests that in the uremic rat, gastric hyperemia, mediated by increased endothelium-derived nitric oxide, attenuates ethanol-induced gastric mucosal injury.

引用

页码：1324 / 1328

页数：5

共 22 条

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