NO合酶抑制剂在多巴胺抑制小鼠胃肠推进运动中的作用

The role of NO biosynthesis inhibitor in dopamine-induced inhibition of mice gastric intestinal motility

目的 研究一氧化氮 (NO)合酶抑制剂L -NG -硝基精氨酸甲酯 (L -NAME)在多巴胺对小鼠胃肠推进运动影响中的作用。方法 将 32只小鼠随机分为 3组 :对照组 (n =6 ) ,静脉注射生理盐水 ;A组 (n =7)静脉注射多巴胺 ;B组 (n =19)静脉分别注射不同剂量的L -NAME ,10min后分别静脉注射多巴胺。采用含 12 %活性炭和4%黄芪胶的炭末胶液灌胃 ,计算 2 0min炭末胶液在小肠内推进距离占小肠全长的百分比 ,以此作为小肠推进速度的指标 ,同时测定灌胃 2 0min后胃内炭末胶液剩余的容积。结果 静脉单独注射多巴胺组与正常对照组相比小肠推进速度减慢 18.0 % ,胃内剩余量增加 85 .2 % ,均有显著性差异 (P <0 .0 1,P <0 .0 5 ) ;静脉预先注射L -NAME 3mg kg可以完全翻转随后给予多巴胺对胃肠推进运动的抑制作用 ;而静脉注射L -NAME(6mg kg和 12mg kg) +多巴胺组 ,与单独注射多巴胺组相比 ,小肠推进速度分别减慢 3.8%和 18.8% ,而胃内剩余量分别增加2 8.8%和 45 .6 % (P <0 .0 5 )。结论 静脉注射多巴胺对小肠推进速度的影响除直接作用于小肠平滑肌细胞外 ,还与胃排空速度有关 ;

Objective To study the role of the NO-biosynthesis inhibitor N-nitro-L-arginine methyl ester (L-NAME) in dopamine(DA)-induced gastrointestinal propulsion of mice.?Methods 32 mice were divided randomly into 3 groups: control group ( n =6) received normal saline intravenously; group A ( n =7) received dopamine intravenously; group B ( n =19) were pretreated with different dosage of L-NAME followed by intravenous dopamine 10 min later, respectively. A mixture of activated charcoal (12%) and gum tragacanth(4%) was perfused into the stomach of mouse. The percentage length of in small intestinal propulsion within 20 minutes was taken to express the intestinal propulsion speed and gastric emptying was assessed by measuring remained volume in the stomach.?Results DA significantly reduced the speed of intestinal propulsion and increased intragastric remained volume compared with those of control ( P <0.01, P <0.05);That DA inhibited The speed of small intestinal propulsion and gastric emptying was reversed by intravenous inhibitor of NO synthesis (L-NAME 3 mg/ kg).Pretreated by intravenous inhibitor of NO synthesis (L-NAME 6 mg/kg or 12 mg/kg), ?the speed of intestinal propulsion reduced by 3.8% and 18.8%, ? intragastric remained volume increased by 28.8% and 45.6% ( P <0.05), respectively.? Conclusion That DA-inhibited small intestinal propulsion may contribute to its delayed gastric emptying. NO is responsible for the DA-mediated small intestinal motility and gastric emptying.