摘要
目的 :探讨内皮素 1在豚鼠乳头肌诱发异常电活动的特征及其离子机制。方法 :用常规微电极技术引导并记录心肌细胞内电活动 ,分析其各参数。结果 :ET 1浓度依赖地延长乳头肌细胞的APD ,并在低Mg2 + 灌流的条件下诱发EADs。ET 1所诱发EADs的幅度、触发发放时程TBD具有明显的浓度依赖性和刺激周长依赖性。ETA 受体拮抗剂BQ 12 3和Ca2 + 通道阻断剂硝苯吡啶可消除ET 1的上述作用。结论 :ET 1通过ETA 受体激活Ca2 + 通道 ,导致细胞内Ca2 + 超载进而诱发EADs。由于EADs的出现 ,致使心肌细胞复极化异常 ,可能是ET 1致心律失常作用的电生理基础。
Objective: Present study focuses on the electrophysiological properties of arrhythmogenic action of endothelin and its underlying mechanisms.Methods: Transmembrane action potential (AP) in guinea pig papillary muscles were recorded with microelectrode and the parmeters of APs were analysed with computer.Results: ET 1 significantly prolonged APD in concentration dependent manner and induced stable EADs at lower concentration of [Mg 2+ ] 0.The occurence of EADs induced by ET 1,their amplitudes and triggered burst duration (TBD) were markdly dependent on the dose and the drive cycle length.Both the prolongation APD and occurence of EADs evoked by ET 1 were abolished by either BQ 123,an ET A receptor selective antagonist,or Nif,a Ca 2+ channel blocker.Conclusion: EADs induced by ET 1 in the papillary muscles might be attributed to intracellular Ca 2+ overloading as result of an activation of Ca 2+ channel via ET A receptor.ET iduced abnormalities of reploarization,as were manifested by EADs,provided an important electrophysiological basis for the occurence of fatal arrhythmia.
出处
《河南医学研究》
CAS
2000年第2期112-115,共4页
Henan Medical Research
基金
河南省医学科学院科研基金
