Renal failure increases gastric mucosal blood flow and acid secretion in rats: role of endothelium-derived nitric oxide.
Renal failure increases gastric mucosal blood flow and acid secretion in rats: role of endothelium-derived nitric oxide.
复制标题
肾衰竭增加大鼠胃粘膜血流量和酸分泌：内皮源性一氧化氮的作用。
DOI：
10.1152/ajpgi.1992.263.1.g75
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Guth,PH
中科院分区：
文献类型：
--
作者：
Quintero,E;Guth,PH
由于临床研究的结果相互矛盾，并且完全缺乏动物研究，本研究的目的是表征慢性肾衰竭动物模型中胃粘膜血流量（GMBF）和酸分泌的变化。部分肾梗死所致慢性肾功能衰竭大鼠的基础GMBF显着高于对照大鼠，胃血管阻力显着降低。肾衰竭大鼠的胃酸分泌和粘膜充血反应对五肽胃泌素显着增强。由于内皮源性一氧化氮（NO）是一种调节胃血管张力的内源性血管扩张剂，我们假设NO介导肾衰竭大鼠的胃充血。 N omega-硝基-L-精氨酸甲酯（L-NAME）是一种NO形成的特异性抑制剂，与对照大鼠相比，肾衰竭大鼠的GMBF显着降低，包括低剂量抑制肾衰竭大鼠的基础充血，但对对照大鼠没有影响。它还减弱了两组中五肽胃泌素刺激的 GBBF。相比之下，L-NAME 使肾衰竭大鼠和对照大鼠的基底骨骼肌血流量出现类似的减少。我们得出结论，在肾衰竭大鼠中：1) 基础 GBF 和五肽胃泌素刺激的酸输出和 GBF 增加，2) 这种胃粘膜充血是由 NO 介导的。
Because of the contradictory findings in clinical studies, and the complete lack of animal studies, the purpose of this investigation was to characterize the changes in gastric mucosal blood flow (GMBF) and acid secretion in an animal model of chronic renal failure. Rats with chronic renal failure induced by partial kidney infarction had a significantly higher basal GMBF and lower gastric vascular resistance than control rats. The gastric acid secretory and mucosal hyperemic response to pentagastrin were markedly enhanced in renal failure rats. Because endothelial-derived nitric oxide (NO) is an endogenous vasodilator that regulates gastric vascular tone, we hypothesized that NO mediates the gastric hyperemia of renal failure rats. The administration of N omega-nitro-L-arginine methyl ester (L-NAME), a specific inhibitor of NO formation, produced a significantly greater decrease in GMBF in renal failure rats than in control rats, including a low dose inhibiting the basal hyperemia in renal failure rats but having no effect in control rats. It also attenuated pentagastrin-stimulated GMBF in both groups. In contrast, L-NAME produced a similar decrease in basal skeletal muscle blood flow in both renal failure and control rats. We conclude that in the renal failure rat 1) there is an increased basal GMBF and pentagastrin-stimulated acid output and GMBF, and 2) this gastric mucosal hyperemia is mediated by NO.