Effect of endothelium-derived relaxing factor on the gastric lesion induced by HCl in rats.
Effect of endothelium-derived relaxing factor on the gastric lesion induced by HCl in rats.
复制标题
内皮源性舒张因子对HCl所致大鼠胃损伤的影响
DOI：
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发表时间：
1990
影响因子：
3.5
通讯作者：
H. Kohei
中科院分区：
文献类型：
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作者：
H. Kitagawa;F. Takeda;H. Kohei
为探讨内皮源性舒张因子（EDRF）对大鼠胃粘膜损伤的影响，本实验观察了盐酸对内皮依赖性胃粘膜血流量增加的影响，以及EDRF抑制剂和亚硝酸盐对盐酸胃粘膜损伤的影响。局部应用0.6 N盐酸对胃粘膜抑制内皮依赖性增加粘膜血流动力学估计使用器官反射分光光度法诱导迷走神经刺激或乙酰胆碱，但不是罂粟碱。胶原酶、棉酚、血红蛋白和抗坏血酸已被报道抑制内皮依赖性血管舒张，抑制迷走神经刺激和乙酰胆碱引起的粘膜血流动力学增加。这些抑制剂和亚甲蓝显着增强0.45 N HCl引起的胃损伤。动脉内或局部应用亚硝酸盐（亚硝酸钠和亚硝酸异戊酯）增加粘膜血流动力学。口服亚硝酸盐可防止0.6 N HCl诱导的胃损伤的形成。提示EDRF在胃粘膜抗盐酸损伤中起重要作用。内皮依赖性的粘膜血流量增加减少可能是大鼠胃粘膜损伤的一个病因。
Effect of HCl on the endothelium-dependent increase in mucosal blood flow and effect of endothelium-derived relaxing factor (EDRF) inhibitors or nitrites on the HCl-induced gastric lesion were studied to clarify the effect of EDRF on the formation of gastric lesion in rats. Topical application of 0.6 N HCl on the gastric mucosa inhibited the endothelium-dependent increase in mucosal hemodynamics estimated using organ-reflectance spectrophotometry induced by vagal stimulation or acetylcholine, but not by papaverine. Collagenase, gossypol, hemoglobin and ascorbic acid have been reported to inhibit the endothelium-dependent vasodilation, inhibited increase in mucosal hemodynamics induced by vagal stimulation and acetylcholine. These inhibitors and methylene blue significantly enhanced the gastric lesion induced by 0.45 N HCl. Intra-arterial or topical application of nitrites (sodium nitrite and isoamyl nitrite) increased mucosal hemodynamics. Oral administration of nitrites prevented the formation of 0.6 N HCl-induced gastric lesion. These results suggest that EDRF plays an important role in the protection of gastric mucosa against HCl. Reduced endothelium-dependent increase in mucosal blood flow may be an etiology of gastric lesion in rats.