腺苷对模拟缺血再灌注豚鼠心室肌细胞动作电位的影响及其离子机制  

Effects of adenosine on action potential and its ionic mechanisms in guinea-pig ventricular myocytes under simulated ischemic-reperfused conditions

作　　者：赵正航[1] 臧伟进[1] 于晓江[1] 孙强[1] 吕军[1] 张春虹[1] 

机构地区：[1]西安交通大学医学院药理学教研室,西安710061

出　　处：《中国药理学通报》2003年第3期274-278,共5页Chinese Pharmacological Bulletin

基　　金：高等学校博士点专项科研基金资助项目No 2 0 0 10 698034;教育部科学技术重点基金资助课题 No 0 1161;国家自然科学基金资助课题No 3 9970 2 73No 3 0 2 70 5 5 4

摘　　要：目的　研究腺苷 (Ado)在模拟缺血缺氧时对豚鼠心室肌细胞动作电位 (AP)、L 型钙电流 (ICa.L)和ATP敏感性钾电流 (IK .ATP)的影响。方法　在离体豚鼠心室肌和酶解法分离的单个豚鼠心室肌细胞上 ,分别应用细胞内微电极和全细胞膜片钳技术记录动作电位和电流。结果　在模拟缺血缺氧状态下 ,Ado剂量依赖性的增大动作电位时程 (APD)的缩短 (P <0 0 5 ) ;抑制再灌注后APD恢复 ,而表现出迟后恢复。在缺血缺氧状态下 ,ICa.L受到抑制 ,Ado并不加重心肌细胞缺血缺氧时ICa.L的减小 ,而再灌注后ICa .L的恢复比较缓慢 ,但同对照组比较无差异。Ado可加速缺血缺氧时IK .ATP的激活 ,Ado(10 0 μmol·L-1)组在缺血缺氧时和再灌注后IK .ATP较对照组均明显增大。结论　在缺血缺氧状态下 ,Ado可增大APD的缩短 ,抑制再灌注后APD的恢复 ,其机制主要在于在缺血缺氧状态下Ado增大了IK .ATP。AIM To investigate the effects of adenosine on action potential (AP), L type calcium channel current ( I Ca.L ), and ATP sensitive potassium current ( I K.ATP ) in guinea pig ventricular myocytes under simulated ischemic reperfused conditions. METHODS Action potential was recorded in guinea pig ventricular myocytes using standard intracellular microelectrode technique. Whole cell patch clamp technique was used to record currents. RESULTS Ado enhanced the abbreviation of APD with a patter of dose dependence in simulated ischemic and hypoxic guinea pig ventricular myocytes,and inhibited the recovery of APD during reperfusion. Under ischemic and hypoxic conditions, the amplitude of I Ca.L was greatly decreased. Ado did not aggravate the decrease of I Ca.L induced by ischemia and hypoxia. Reperfusion was accompanied by a slow return of I Ca.L toward preischemic values. Ado accelerated the activation of I K.ATP in ischemia. Values of I K.ATP in Ado (100 μmol·L -1 ) group were greater than that of control in both ischemia and reperfusion. CONCLUSION Ado significantly increased the abbreviation of APD in guinea pig ventricular myocytes under simulated ischemic and hypoxic conditions and delayed recovery of APD in reperfusion. The mechanism of effects of Ado on APD in ischemia and reperfusion was attributed to the increase in I K.ATP .

关 键 词：腺苷 膜片钳技术 心室肌细胞 模拟缺血缺氧 动作电位 钙电流 ATP敏感的K^+电流 

分 类 号：R542.2[医药卫生—心血管疾病]