腺苷对正常及模拟缺血缺氧状态下豚鼠心肌细胞动作电位及L型钙通道电流的影响

目的　研究腺苷 (Ado)在正常和缺血缺氧时对心室肌细胞跨膜动作电位 (AP)和L 型钙电流 (ICa .L)的影响。方法　用离体心室肌和酶解法分离得到单个豚鼠心室肌细胞 ,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　Ado对正常心室肌跨膜动作电位无明显影响 ,但在缺血缺氧状态下 ,动作电位时程(APD)各参数的缩短较对照组更显著 ,Ado在 10 0 μmol·L-1时 ,APD各参数的缩短程度同对照组比较具有显著性差异 (P <0 0 1)。再灌注后APD未能恢复到原来的水平 ,而表现出的明显的迟后恢复。Ado对正常心室肌细胞ICa .L无明显影响 ;在缺血缺氧时ICa.L受到明显抑制 ,其抑制率为 (38± 11) % ,再灌注后ICa .L可基本恢复 ;而Ado并无增大心肌细胞在缺血缺氧时ICa.L减小的作用 ,其抑制率为 (42± 9) % ,但无明显统计学意义 (P >0 0 5 ) ,而再灌注后ICa.L的恢复比较缓慢。结论　①Ado在正常条件下对豚鼠心室肌细胞动作电位和ICa.L无明显作用 ;②Ado在缺血缺氧时可使APD的缩短明显增大 ,再灌注时APD恢复明显延迟 ;③Ado并不能加重心肌在缺血时ICa .L的减小 ;④心肌缺血缺氧时Ado增大APD的缩短与ICa .L的变化可能无明显平行关系

Effects of adenosine on action potential and L-type calcium channel current in Guinea-pig ventricular myocytes under normal and imitated ischemia-reperfusion conditions

Objective To investigate the effects of adenosine on action potential (AP) and L type calcium channel current (I Ca.L ) in Guinea pig ventricular myocytes in normal and simulated ischemia reperfusion 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 I Ca.L .Results Ado had no direct effect on the AP in Guinea pig ventricular myocytes under normal conditions. However, it abbreviated the parameters of APD under simulated ischemia and hypoxia conditions. At the concentration of Ado 100?μmol·L -1 , APD 30 , APD 50 , and APD 90 were significantly reduced compared with those of control after ventricle was superfused with simulated ischemic Tyrode's solution for 15 minutes ( P <0.01). During reperfusion AP parameters did not completely return to initial values in the presence of Ado. Ado had no effect on myocytes under normal conditions. Under ischemic and hypoxic conditions, the peak amplitude of I Ca.L at 0mV decreased by (38±11)% compared with that of control. With Ado present in ischemia, I Ca.L decreased by (42±9)% compared with that of control, and there was no significant difference between that of the two groups. In Addition, Ado had no significant effect on maximum active voltage.Conclusion Ado has no significant effects on the AP and I Ca.L in Guinea pig ventricular myocytes under normal conditions, but it significantly abbreviates APD under ischemic and hypoxic conditions and delays recovery of APD in reperfusion. Ado cannot aggravate the decrease of I Ca.L . This effect of Ado on APD in ischemia and (or) reperfusion may not have significantly parallel relationship with I Ca.L .