内源性一氧化氮在高血糖抑制大鼠胃肠推进运动中的作用  

Effects of Endogenous Nitric Oxide on Gastrointestinal Propulsive Motility Inhibited by Hyperglycemia in Rats

作　　者：余贤恩 黎建绿[1,2] 晋玲[1,2] 黄丽娟[1,2] 杨有业[1,2] 

机构地区：[1]广西百色地区人民医院消化内科 [2]右江民族医学院生理教研室

出　　处：《基础医学与临床》1997年第4期57-60,共4页Basic and Clinical Medicine

摘　　要：用墨粉胶液在大鼠胃肠内推进距离占胃肠全长的百分数，作为胃肠推进运动的指标，观察了经尾静脉注射高浓度葡萄糖、ＮＧ－硝基－Ｌ－精氨酸甲酯（Ｌ－ＮＡＭＥ）及Ｌ－精氨酸（Ｌ－ＡＲＧ）对这一推进运动的影响。２０％葡萄糖明显抑制胃肠推进运动，而Ｌ－ＮＡＭＥ可对抗２０％葡萄糖而明显增加胃肠推进运动。预先应用Ｌ－ＡＲＧ可以翻转Ｌ－ＮＡＭＥ的作用。上述结果表明：（１）高血糖明显抑制大鼠胃肠推进运动，（２）内源性一氧化氮至少部分中介了高血糖的这种抑制作用。The effects of intravenous injections of high concentration glucose,L nitro arginine methyl ester (L NAME) and L arginine (L ARG) on the gastrointestinal propulsive motility were studied in rats.The distance travelled by toner meal through the gastrointestinal tract,measured in terms of percentage of its total lenght,was recorded as the index of propulsive motility.The results were as follows: (1)20% glucose very significantly inhibited the gastrointestinal propulsive motility (p<0.01). (2) L NAME very significantly increased the gastrointestinal propulsive motility against 20% glucose (p<0 01). (3) The above effect of L NAME on gastrointestinal propulsive motility could be reversed by pretreatment with L ARG (p<0.05) The results indicate: (1) Hyperglycemia very significantly inhibited gastrointestinal propulsive motility in rats. (2) Endogenous nitric oxide,at least partly,mediated this inhibitory effect of hyperglycemia.

关 键 词：高血糖 胃肠推进运动 一氧化氮 糖尿病 

分 类 号：R587.102[医药卫生—内分泌]