内源性－氧化氮对大鼠胃粘膜血流量和胃粘膜损伤的影响

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。

EFFECT OF ENDOGENOUS NITRIC OXIDE ON GASTRIC MUCOSAL BLOOD FLOW AND GASTRIC MUCOSAL LESION IN RATS

By hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF), role of nitric oxide (NO) in the gastric mucosal lesion and hyperemic reponse to gastric perfusion with 15% ethanol in 0.15 mol/L HCl was investigated, The results were as follows:(1)there was an increase in gastric mucosal lesion associated with a hyperemic response to intragastric 15% ethnol in 0.15mol/L HCl;(2) the gastric hyperemic response to intragastric 15% ethanol in 0.15mol/L HCl was blocked by the pretreatment with L-nitro-arginine methyl ester (L-NAME), which significantly increased the gastric mucosal lesion and arterial blood pressure;(3) pretreatment with methylene blue attenuated the increase of GMBF and augmented the gastric mucosal lesions induced by gastric perfusion with 15% ethanol in 0.15mol/L HCl. These results show that the increased GMBF induced by gastric perfusion with ethanol in HCl, which enhances the gastric cytoprotection, is mediated by NO.