环维黄杨星D抗心房纤颤的作用及其电生理机制  

ANTI ATRIAL FIBRILLATION EFFECTS OF CYCLOVIROBUXINE D AND ITS ELECTROPHYSIOLOGICAL MECHANISM STUDIED ON GUINEA PIG ATRIA

作　　者：汪永孝[1] 郑云敏 谭月华[1] 盛宝恒 

机构地区：[1]第四军医大学药理教研室 空医系

出　　处：《药学学报》1996年第7期481-486,共6页Acta Pharmaceutica Sinica

摘　　要：环维黄杨星Ｄ（ＣＶＢＤ）对ＣａＣｌ２Ａｃｈ诱发小鼠在体心房纤颤和乌头碱、哇巴因或肾上腺素所致豚鼠离体心房纤颤，有明显的剂量依赖性抑制作用，且作用强度与胺碘酮（Ａｍｉ）相似。ＣＶＢＤ０．３～１００μｍｏｌ·Ｌ－１降低离体右心房自律性。对离体左心房，ＣＶＢＤ０．３μｍｏｌ·Ｌ－１抑制肾上腺素引起的异常自律性，延长有效不应期和动作电位时程，降低兴奋性；高浓度时，可降低Ｖ·ｍａｘ，延长冲动传导时间。Ａｍｉ０．３～３０μｍｏｌ·Ｌ－１有相似的电生理作用，但对Ｖ·ｍａｘ无明显的影响。Cyclovirobuxine D (CVB D) was shown to produce significant and dose dependent protective effects against atrial fibrillation induced by CaCl 2 Ach in mice. On atrial fibrillation induced by aconitine, ouabain or adrenaline in isolated guinea pig atria, the effects of CVB D were similar to those of amiodarone. CVB D 0.3～100 μmol·L -1 was shown to depress the automaticity of the isolated guinea pig right atria. In isolated left atria, CVB D 0.3 μmol·L -1 was found to inhibit the abnormal automaticity elicited by adrenaline, to prolong the duration of action potential and effective refractory period and to reduce excitability. At high concentration (30 μmol·L -1 ), CVB D was also found to decrease the maximal velocity of depolarization (V· max ) and to elongate the conduction time of initiation. Amiodarone 0.3～30 μmol·L -1 was shown to closely resemble CVB D in electrophysiology without effect on V· max .

关 键 词：环维黄杨星D 胺碘酮 心房纤颤 抗心律失常药 

分 类 号：R972.2[医药卫生—药品] R541.750.5[医药卫生—药学]