甲基莲心碱对氧自由基介导冠状血管阻力变化的影响  

Efectofneferineonchangeofcoronaryvascularresistanceinducedbyoxygenfreradicalsinisolatedrathearts

作　　者：吴远明[1] 胡本蓉[1] 贾菊芳[1] 

机构地区：[1]同济医科大学药理学教研室

出　　处：《中国药理学与毒理学杂志》1996年第2期116-119,共4页Chinese Journal of Pharmacology and Toxicology

摘　　要：研究了甲基莲心碱（Ｎｅｆ）对氧自由基介导离体大鼠冠状血管阻力变化的影响．结果发现电解性氧自由基可引起冠脉灌注压（ＣＡＰＰ）增加；去冠状血管内皮后，电解所致ＣＡＰＰ的增加明显减弱．预先给予Ｌ－精氨酸（１００μｍｏｌ·Ｌ－１）能明显对抗氧自由基所致的ＣＡＰＰ增加，且Ｌ－精氨酸的作用能部分被硝基－Ｌ－精氨酸（２００μｍｏｌ·Ｌ－１）所对抗，提示电解所致ＣＡＰＰ的增加与氧自由基影响冠状血管内皮功能有关．Ｎｅｆ依剂量性地对抗电解所致ＣＡＰＰ的增加，且Ｎｅｆ（１０μｍｏｌ·Ｌ－１）的作用能被硝基－Ｌ－精氨酸（２００μｍｏｌ·Ｌ－１）或吲哚美辛（１μｍｏｌ·Ｌ－１）所对抗，提示Ｎｅｆ的作用可能部分通过影响前列腺素及内皮源性舒张因子类物质的代谢有关．Efectofneferineonchangeofcoro-naryvascularresistanceinducedbyoxygenfreeradi-calsintheisolatedratheartswasstudied.Experi-mentalresultsshowedthatoxygenfreeradicals,gen-eratedbyelectrolysisofthephysiologicalperfusate,couldinduceaprogressiveincreaseofcoronaryperfu-sionpressure(CAPP)inrathearts.Afterremovingcoronaryvascularendothelialcels,theincreaseofCAPPinducedbyelectrolysiswasatenuatedsignifi-cantly.L-Arginine(100μmol·L-1),anendoge-nousnitricoxideprecursor,couldpreventtheCAPPincreaseelicitedbyelectrolysis,andtheefectofL-argininewaspartlyreducedbyNω-nitro-L-argi-nine(200μmol·L-1),anitricoxidesynthetasein-hibitor.TheresultsuggeststhattheCAPPincreaseinducedbyelectrolysismaybeassociatedwiththein-fluenceofoxygenfreeradicalsoncoronaryvascularendothelialfunction.Neferine,abisbenzyliso-quinolinealkaloid,couldpreventCAPPincreasedose-dependentlyandtheefectofneferine(10μmol·L-1)waspartlyinhibitedbyNω-nitro-L-arginine(200μmol·L-1)orindometacin(1μmol·L-1).Theseresultsindicatethattheefectofneferinemaybepartlyrelatedtothemetabolismofendothelium-derivedrelaxingfactororprostaglandin-likesub-stance.

关 键 词：甲基莲心碱 自由基 冠状血管 

分 类 号：R972[医药卫生—药品]