3-Morpholinosydnonimine-N-ethylcarbamide对缺氧诱发离体猪冠脉机械和电反应的影响(英文)  

Effects of 3-morpholinosydnonimine-N-ethylcarbamide on hypoxia-induced mechanical and electric responses of isolated pig coronary artery

作　　者：杨小平[1] 王福旭[1] 任德成 吕士臣 傅绍萱[1] 李蕴山[1] 

机构地区：[1]河北医学院药理教研室

出　　处：《中国药理学报》1995年第6期494-496,共3页Acta Pharmacologica Sinica

基　　金：Natural Science Foundation of Hebei Province, №393126.

摘　　要：研究3-Morpholinosydnonimine-N-ethylcarbamide(SIN-1)对缺氧诱发离体猪冠脉机械和电反应的影响.方法:同步记录机械张力和膜电位.结果:缺氧可诱发离体猪冠脉平滑肌细胞膜去极化和收缩;SIN-1(100 μmol·L^(-1))和维拉帕米(Ver,10 μLmol·L^(-1))可使其复极化和松弛.SIN-1和Ver还可抑制左旋硝基精氨酸(NLA,0.2 mmol·L^(-1))和KCl(40mmol·L^(-1))诱发的离体猪冠脉去极化和收缩反应.结论:缺氧收缩离体猪冠脉是其抑制一氧化氮释放、增加Ca^(2+)内流的结果.To study effects of 3-morpholi-nosydnonimine-N-ethylcarbamide (SIN-1) on hypoxia-induced mechanical and electric activities of the isolated pig coronary artery. METHODS: Mechanical tension and membrane potential were measured simultaneously. RESULTS:Hypoxia initially caused a transient vascular smooth muscle cell membrane hyperpolarization followed by a membrane depolarization in isolated pig coronary artery. Subsequent addition of SIN-1 100 μmol·L-1 or verapamil (Ver) 10μmol·L-1 led to membrane repolarization and relaxation of the vascular smooth muscle. Nitro-L-arginine (NLA) 0.2 mmol·L-1 and KCl 40 mmol·L-1 also induced membrane depolarization and vasoconstriction, which were similarly suppressed by SIN-1 or Ver. CONCLUSION: Hypoxic contractile response in isolated pig coronary artery is mediated by an increased Ca2+ influx via suppression of nitric oxide release.

关 键 词：一氧化氮 维拉帕米 膜电位 冠状血管 缺氧症 

分 类 号：R965.2[医药卫生—药理学]