Li G R, Ferrier G R, Howlett S E
Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada.
Am J Physiol. 1995 Mar;268(3 Pt 2):H999-1005. doi: 10.1152/ajpheart.1995.268.3.H999.
Possible changes in Ca2+ currents (ICa), which might contribute to Ca2+ overload in young (70- to 100-day-old) cardiomyopathic (CM) hamster hearts, were determined in isolated ventricular myocytes with conventional recording and discontinuous single-electrode voltage-clamp techniques. Action potential duration at 90% repolarization (APD90) was significantly longer in CM myocytes compared with normal cells (APD90 = 120.3 +/- 4.5 vs. 98.2 +/- 5.9 ms, P < 0.01). Input resistance, membrane time constant, and membrane capacitance were similar in normal and CM myocytes. Current-voltage (I-V) relations for peak ICa were depressed in CM cells compared with normal cells; this difference was statistically significant at the peak of the I-V curve. Activation and inactivation relations for ICa and recovery from inactivation were similar in myocytes from normal and CM hearts. These changes occurred in myocytes from young CM animals before development of heart failure. Results indicate that increased Ca2+ influx through L-type Ca2+ channels does not account for the longer APD in cardiomyopathy and is not involved in the development of Ca2+ overload in cardiomyopathy.
利用传统记录和间断单电极电压钳技术，在分离的心室肌细胞中测定了可能导致年轻（70至100日龄）心肌病（CM）仓鼠心脏中Ca2+超载的Ca2+电流（ICa）变化。与正常细胞相比，CM心肌细胞中90%复极化时的动作电位时程（APD90）显著延长（APD90 = 120.3±4.5对98.2±5.9毫秒，P < 0.01）。正常和CM心肌细胞的输入电阻、膜时间常数和膜电容相似。与正常细胞相比，CM细胞中ICa峰值的电流-电压（I-V）关系降低；这种差异在I-V曲线峰值处具有统计学意义。正常和CM心脏的心肌细胞中，ICa的激活和失活关系以及失活后的恢复情况相似。这些变化发生在年轻CM动物出现心力衰竭之前的心肌细胞中。结果表明，通过L型Ca2+通道增加的Ca2+内流不能解释心肌病中较长的APD，并且不参与心肌病中Ca2+超载的发生。
