腺苷拮抗ISO对豚鼠心室肌细胞动作电位及内向整流钾通道作用机制的探讨

摘要

目的：探讨腺苷(ADO)拮抗异丙基肾上腺素(ISO)对豚鼠乳头肌动作电位和心室肌细胞内向整流钾通道电流(Inward rectifier potassium currents，IK1)的影响，阐明IK1在儿茶酚胺增高性室性心动过速中的作用机制及ADO治疗的离子流基础。方法：采用标准玻璃微电极及全细胞膜片钳方法，分别记录ISO，ISO加腺苷对豚鼠乳头肌动作电位及心室肌细胞IK1影响。结果：ISO延长动作电位时程(APD)，诱发早期后除极(EAD)，延迟后除极(DAD)及触发激动，增加L型-钙电流(ICa-L)及Ik1。ADO抑制ISO所致APD延长，并抑制I k1、ICa-L。腺苷A1受体阻断剂(DPCPX)拮抗ADO的作用。结论：IK1开放减弱ISO所致的APD延长，对心肌细胞具有保护作用。ADO拮抗ISO对APD的影响，与抑制ICa-L、Ik1有关。%Objective: To investigate the mechanism of adenosine antagonized isoproterenol on action potentials and inward rectifierpotassium channels in guinea pig papillary muscles and ventricular myocytes, and to demonstrate the ionic current basic inthe treatment with adenosine. Methods:Standard glass microelectrode method and whole cell patch clamp techniques wereused to study the effect of adenosine on action potential and Ica-L, IKl. Results: ISO prolonged APD, urged EAD, delayed DADand triggered activity, and increased ICa-L and IKi. APD prolongation caused by ISO, and Iki, and Ica-L were inhibited byADO. The effect of ADO was antagonized by DPCPX. Conclusion: Openings of IKl may shorten APD with the protection formyocytes. There is a correlation between the effect of ADO to APE caused by the antagonized effect to ISO and Ica-L and Iklinhibition.