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一氧化氮参与胃血流量和组织氧合的调节。

Nitric oxide is involved in the mediation of gastric blood flow and tissue oxygenation.

作者信息

Gustaw P, Pawlik W W, Czarnobilski K, Sendur R, Konturek S J

机构信息

Institute of Physiology, Jagiellonian University School of Medicine, Cracow, Poland.

出版信息

J Physiol Pharmacol. 1994 Sep;45(3):361-8.

PMID:7841449
Abstract

Endogenous nitric oxide which is enzymatically formed by endothelial cells from L-arginine has been implicated in the control of gastrointestinal circulation. Its role in the mediation of gastric tissue oxygenation has not been studied. We investigated the role of NO in the control of gastric blood flow and oxygen uptake. In anesthetized dogs, total gastric blood flow, gastric mucosal blood flow, systemic arterial and portal venous pressures and the arteriovenous oxygen content difference were studied. From these measurements gastric vascular resistance and oxygen consumption were calculated. Administration of NG-nitro-L-arginine (L-NNA) induced gastric tissue ischemia and hypoxia. Both, systemic arterial pressure and gastric vascular resistance were increased. Above hemodynamic and metabolic effects of L-NNA were significantly attenuated when administration of L-NNA was combined with L-arginine. Our findings suggest that endogenous NO is a tonic vasodilator modulating gastric blood flow and oxygen uptake through influence on the gastric microcirculatory structures responsible for vascular resistance and the nutrient circulation.

摘要

内源性一氧化氮由内皮细胞通过L-精氨酸酶促生成,已被认为参与胃肠道循环的调控。其在介导胃组织氧合中的作用尚未得到研究。我们研究了一氧化氮在控制胃血流量和氧摄取中的作用。在麻醉犬中,研究了总胃血流量、胃黏膜血流量、体动脉和门静脉压力以及动静脉氧含量差。通过这些测量计算出胃血管阻力和氧耗量。给予NG-硝基-L-精氨酸(L-NNA)可导致胃组织缺血和缺氧。体动脉压和胃血管阻力均升高。当L-NNA与L-精氨酸联合给药时,L-NNA的上述血流动力学和代谢效应明显减弱。我们的研究结果表明,内源性一氧化氮是一种维持性血管舒张剂,通过影响负责血管阻力和营养物质循环的胃微循环结构来调节胃血流量和氧摄取。

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