中国药理学与毒理学杂志
中國藥理學與毒理學雜誌
중국약이학여독이학잡지
CHINESE JOURNAL OF PHARMACOLOGY AND TOXICOLOGY
2005年
1期
13-17
,共5页
李茜%刘苏%陈子英%刘宜先%张文立%赵宏%刘林立%何瑞荣
李茜%劉囌%陳子英%劉宜先%張文立%趙宏%劉林立%何瑞榮
리천%류소%진자영%류의선%장문립%조굉%류림립%하서영
辣椒素%心房%电生理学%钙
辣椒素%心房%電生理學%鈣
랄초소%심방%전생이학%개
capsaicin%heart atrium%electrophysiology%calcium
目的研究辣椒素对人心房肌的电生理效应及其作用机制.方法应用经典玻璃微电极方法记录人心房肌特殊细胞的动作电位.结果辣椒素(1~30 μmol·L-1)浓度依赖性地抑制人心房肌纤维的动作电位幅值,0期最大除极速率,舒张期(4相)除极化速率和起搏细胞放电频率,此外还缩短90%动作电位时程.应用L-型钙通道开放剂Bay K8644(0.5 μmol·L-1)可拮抗辣椒素对人心房肌纤维的上述电生理效应, 但辣椒素受体竞争性抑制剂capsazepine(10 μmol·L-1)对辣椒素的效应并无影响.结论辣椒素对人心房肌具有负性变时作用,并可缩短复极化时程.这些效应可能与其抑制钙离子内流有关.
目的研究辣椒素對人心房肌的電生理效應及其作用機製.方法應用經典玻璃微電極方法記錄人心房肌特殊細胞的動作電位.結果辣椒素(1~30 μmol·L-1)濃度依賴性地抑製人心房肌纖維的動作電位幅值,0期最大除極速率,舒張期(4相)除極化速率和起搏細胞放電頻率,此外還縮短90%動作電位時程.應用L-型鈣通道開放劑Bay K8644(0.5 μmol·L-1)可拮抗辣椒素對人心房肌纖維的上述電生理效應, 但辣椒素受體競爭性抑製劑capsazepine(10 μmol·L-1)對辣椒素的效應併無影響.結論辣椒素對人心房肌具有負性變時作用,併可縮短複極化時程.這些效應可能與其抑製鈣離子內流有關.
목적연구랄초소대인심방기적전생리효응급기작용궤제.방법응용경전파리미전겁방법기록인심방기특수세포적동작전위.결과랄초소(1~30 μmol·L-1)농도의뢰성지억제인심방기섬유적동작전위폭치,0기최대제겁속솔,서장기(4상)제겁화속솔화기박세포방전빈솔,차외환축단90%동작전위시정.응용L-형개통도개방제Bay K8644(0.5 μmol·L-1)가길항랄초소대인심방기섬유적상술전생리효응, 단랄초소수체경쟁성억제제capsazepine(10 μmol·L-1)대랄초소적효응병무영향.결론랄초소대인심방기구유부성변시작용,병가축단복겁화시정.저사효응가능여기억제개리자내류유관.
AIM To study the electrophysiological effects of capsaicin on human atrial fibers. METHODS Parameters of action potential in human atrial specialized fibers were recorded using standard intracellular microelectrode technique. RESULTS Capsaicin (1-30 μmol·L-1) decreased the amplitude of action potential, maximal rate of depolarization, velocity of diastolic (phase 4) depolarization and rate of pacemaker firing, and shortened the 90% action potential duration in a concentration-dependent manner. L-type Ca2+ channel agonist Bay K8644 (0.5 μmol·L-1) antagonized the inhibitory effects of capsaicin on human atrial fibers. Pretreatment of the fibers with capsazepine (10 μmol·L-1), a competitive capsaicin antagonist, failed to influence the electrophysiological effects of capsaicin. CONCLUSIONCapsaicin exerted a negative chronotropic action and accelerated the repolarization of human atrial specialized fibers which may be due to reduction in calcium influx and not mediated by capsaicin receptors.