INTRACELLULAR CALCIUM HANDLING IN ISOLATED VENTRICULAR MYOCYTES FROM PATIENTS WITH TERMINAL HEART-FAILURE
INTRACELLULAR CALCIUM HANDLING IN ISOLATED VENTRICULAR MYOCYTES FROM PATIENTS WITH TERMINAL HEART-FAILURE
复制标题
DOI：
10.1161/01.cir.85.3.1046
复制
发表时间：
1992-03-01
期刊：
影响因子：
37.8
通讯作者：
ERDMANN, E
中科院分区：
文献类型：
--
作者：
BEUCKELMANN, DJ;NABAUER, M;ERDMANN, E
背景在人心室肌细胞中进行实验，以研究终末期心力衰竭患者的兴奋-收缩偶联特性。从接受移植的扩张型或缺血性心肌病引起的心力衰竭患者的左心室心肌分离心肌细胞。这些结果进行了比较，从健康供体心脏的细胞，由于技术原因，不适合移植。[Ca2在用Ca 2+指示剂fura 2内部灌注的电压钳下，从分离的细胞记录[Ca 2 +]i瞬变和Ca 2+电流。在外部刺激的细胞中，使用指示剂fura 2-AM的细胞渗透形式。当记录动作电位时，以电流钳模式刺激细胞。肌病细胞和对照细胞中未刺激的Ca 2+电流密度没有显着差异。在患病的心肌细胞中，静息[Ca 2 +]i水平为165 +/- 61 nmol/l，而正常细胞为95 +/- 47 nmol/l。移液器中Na+浓度为5 mmol/l时，峰值[Ca 2 +]i瞬变分别为367 +/- 109和746 +/- 249 nmol/l。肌病变细胞[Ca 2 +]i下降速度明显慢于对照细胞。这是一个延长的动作电位和减少钙螯合的肌浆网的结果。结论。这些结果可以部分解释心力衰竭患者在体心肌收缩力的改变。
Background. Experiments were performed in human ventricular myocytes to investigate properties of excitation-contraction coupling in patients with terminal heart failure. Myocytes were isolated from left ventricular myocardium of patients with cardiac failure caused by dilated or ischemic cardiomyopathy undergoing transplantation. These results were compared with those obtained from cells of healthy donor hearts that for technical reasons were not suitable for transplantation.Methods and Results. [Ca2+]i transients and Ca2+ currents were recorded from isolated cells under voltage clamp perfused internally with the Ca2+ indicator fura 2. In cells that were stimulated externally, the cell-permeant form of the indicator, fura 2-AM, was used. When action potentials were to be recorded, cells were stimulated in current clamp mode. Unstimulated Ca2+ current densities were not significantly different in myopathic and control cells. In diseased myocytes, resting [Ca2+]i levels were 165 +/- 61 nmol/l, compared with 95 +/- 47 nmol/l in normal cells. With 5 mmol/l Na+ in the pipette, peak [Ca2+]i transients were 367 +/- 109 and 746 +/- 249 nmol/l, respectively. The decline of [Ca2+]i during diastole was significantly slower in myopathic cells than in control cells. This was a result of a prolongation of the action potential and of a reduced Ca2+ sequestration by the sarcoplasmic reticulum.Conclusions. These results may partly explain the alterations of contractility in vivo in patients with heart failure.