论文部分内容阅读
采用氢气清除法测定胃粘膜血流量（ＧＭＢＦ），以１％利多卡因消除胃粘膜传入信息，以Ｌ－ｎｉｔｒｏ－ａｒｇｉｎｉｎｅｍｅｔｈｙｌ－ｅｓｔｅｒ（Ｌ－ＮＡＭＥ）阻断内源性一氧化氮（ＮＯ）生物合成，研究大鼠胃内灌注低浓度盐酸乙醇后，灌注高浓度盐酸乙醇引起的胃粘膜血流适应性增多反应中，是否有胃粘膜传入信息和ＮＯ参与。结果：①若先以低浓度盐酸乙醇随之再以高浓度盐酸乙醇灌注，则胃粘膜呈现适应性保护现象，损伤面积和损伤深度分别比单独高浓度组减少４８．６８％和３７．９０％（Ｐ＜０．０１，Ｐ＜０．０５）；同时ＧＭＢＦ出现适应性增加反应，比单独高浓度组增加３８．５３％（Ｐ＜０．０５）；②胃内灌注１％利多卡因或静脉注射ＮＯ生物合成阻断剂Ｌ－ＮＡＭＥ后，ＧＭＢＦ的适应性增加反应被阻断，同时胃粘膜适应性保护作用消失。结果表明，低浓度盐酸乙醇作为弱刺激引起的适应性保护作用中ＧＭＢＦ适应性增加可能是通过感觉传入神经和内源性ＮＯ中介实现的。
Gastric mucosal blood flow (GMBF) was measured by hydrogen scavenging method, the gastric mucosal afferent information was eliminated by 1% lidocaine, and endogenous nitric oxide (NO) was blocked by L-nitro-arginine methyl ester Biosynthesis, to study gastric gastric perfusion with low concentration of ethanol, perfusion of high concentration of hydrochloric acid ethanol induced gastric mucosal blood flow adaptive response, whether gastric mucosal afferent information and NO involved. Results: ① If the low concentration of hydrochloric acid ethanol followed by high concentration of hydrochloric acid ethanol perfusion, the gastric mucosa showed adaptive protection, damage area and depth of injury were reduced by 48.68% and 37.90% (P <0.01, P <0.05). At the same time, GMBF appeared adaptively increased response, which increased by 38.53% (P <0.05) Intravenous NO biosynthesis blocker L-NAME, GMBF increased adaptive response was blocked, while gastric mucosal adaptive protective effect disappeared. The results indicate that the adaptive increase of GMBF in low concentration ethanolic ethanol as a weak stimulus may be mediated by sensory afferent nerves and endogenous NO mediators.