绝对不应期电刺激对正常豚鼠和慢性心力衰竭豚鼠心室肌细胞动作电位及钠离子-钙离子交换的影响

Effects of Electrical Stimulation Applied During Absolute Refractory Period on Action Potential Duration and Na^+-Ca^(2+) Exchange Currents of Ventricular Myocytes From Normal and Failing Guinea-Pigs

目的:探讨绝对不应期电刺激(ARPES)对正常豚鼠和慢性心力衰竭(衰竭)豚鼠心窀肌细胞动作电位(AP)及钠离子—钙离子(Na^+-Ca^(2+))交换的影响。方法:应用膜片钳技术中电流钳记录 ARPES 对 AP 时程的影响,再以不同的 AP 电压钳记录细胞膜 Na^+-Ca^(2+)交换电结果:①ARPES 延长 AP 时程,以 APD_(30)最为显著(P<0.01),差异有统计学意义。②与正常豚鼠心室肌细胞比较,衰竭豚鼠心室肌细胞 AP 的平台期明显不同,表现在 APD_(90)变化(P<0.05)及 APD_(50)变化(P<0.01),差异有统计学意义。③分别以基础刺激(S_t)下的 AP(AP_(S1))和 ARPES 下的 AP(AP_(ARPES))为测试电压,记录 AP 电压钳下的细胞膜 Na^+-Ca^(2+)交换电流,在正常豚鼠心空肌细胞,AP_(ARPES)电压钳记录的单位膜电容下的外向电流强度的帑合值高于 AP_(S1)电压钳记录的相应值,而单位膜电容下的内向电流强度的整合值无显著变化。在衰竭豚鼠心室肌细胞,AP_(ARPES)电压钳记录的单位膜电容下的外向电流强度的整合值明显高于 AP_(S1)电压钳记录的相应值,而单位膜电容下的内向电流强度的整合值无显著变化。外向电流峰值的增加更为明显。结论:ARPES 延长正常豚鼠和衰竭豚鼠心室肌细胞 AP 时程,对心室肌细胞膜 Na^+-Ca^(2+)交换电流的影响可能是其增强整体心脏收缩功能的机制之一。

Objective：To investigate the effects of electrical stimu｜ation applied during absolute refractory period（ARPES） on the action potential duration（APD） and Na^＋ -Ca^2＋ exchange of normal and failing ventricular myocytes from guinea-pigs. Methods：The action potential durations were recorded by whole-cell membrane current clamp, and Na^＋ -Ca^2＋ exchange currents were recorded using action potential（AP） clamp. Results ： （1）ARPES could extend APD30, APD50 and APD90 of normal and failing guinea-pig ventricular myocytes, with APD30 being the most striking（ P 〈 0. 01 ）. （2）With the potential clamp vohage-clamp protocol, the Na^＋ -Ca^2＋ exchange current was recorded. In both normal and failing ventricular myocytes, the integrated reverse Na^＋ -Ca^2＋ exchange current per membrane capacitance increased after APARPES voltage-clamp compared to APS1 vohage-clamp（P 〈 0. 01 ）,whereas the integrated Na^＋-Ca^2＋ exchange current per membrane capacitance were not different. Conclusion ： ARPES prolonged APD of ventricular myocytes from guinea-pigs, and it might effect Na^＋-Ca^2＋ exchange current of normal and failing ventricular myocytes from guinea-pigs which might be one of the mechanisms leading to contractility enhaneement of whole heart by ARPES.