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采用氢气清除法测定胃粘膜血流量（ＧＭＢＦ），观察内源性一氧化氮（ＮＯ）在大鼠胃内灌注０．１５ｍｏｌ／Ｌ ＨＣｌ＋１５％乙醇对ＧＭＢＦ和胃粘膜损伤影响中的作用。结果表明：（１）单纯胃内灌注０．１５ｍｏｌ／ＬＨＣｌ＋１５％乙醇后ＧＭＢＦ增加，胃粘膜损害程度较轻；（２）预先静脉注射ＮＯ生物合成抑制剂Ｌ－ｎｉｔｒｏ－Ｌ－ａｒｇｉｎｉｎｅｍｅｔｈｙｌｅｓｔｅｒ（Ｌ－ＮＡＭＥ）可阻断胃内盐酸酒精引起的ＧＭＢＦ增加效应，并使胃粘膜损伤加重，动脉血压升高；（３）预先静脉注射鸟苷酸环化酶抑制剂美蓝同样可阻断胃内盐酸酒精引起的ＧＡＢＦ增加效应并使胃粘膜损伤加重。以上结果提示：胃内灌注盐酸酒精后ＧＭＢＦ增加对胃粘膜的保护作用是由内源性ＮＯ介导的。
Gastric mucosal blood flow (GMBF) was measured by hydrogen scavenging method. The effect of endogenous nitric oxide (NO) infused with 0.15mol / L HCl + 15% ethanol on the gastric mucosal lesion in rats was observed. The results showed that: (1) GMBF was increased after gastric perfusion with 0.15mol / LHCl + 15% ethanol alone, and gastric mucosal lesion was lesser; (2) NO-biosynthesis inhibitor L-nitro-L-argininemethylester ) Can block the increase of GMBF induced by hydrochloric acid in the stomach and increase the damage of gastric mucosa and increase of arterial blood pressure. (3) Pre-intravenous injection of guanylate cyclase inhibitor methylene blue also blocks gastric acid alcohol GABF caused by increased effects and increased gastric mucosal injury. The above results suggest that the protective effect of GMBF on the gastric mucosa after gastric perfusion with hydrochloric acid is mediated by endogenous NO.