Pierce G N, Rich T L, Langer G A
Department of Medicine, University of California, Los Angeles, School of Medicine.
Circ Res. 1987 Dec;61(6):805-14. doi: 10.1161/01.res.61.6.805.
The purpose of this study was to examine the movements of Ca2+ into the myocardium from the extracellular space during the course of muscle contraction. Equilibration of the rabbit right ventricular wall with perfusate containing 45Ca was measured by collecting effluent droplets over time. This protocol was carried out in a quiescent muscle and then repeated 15-20 minutes later in an identical fashion except that halfway through the collection period the muscle was stimulated to contract. We were thus able to quantitate the contraction-dependent changes in 45Ca movements. In control experiments using [58Co]EDTA as an extracellular space marker, we observed that contraction altered the volume of this space. This alteration in extracellular space was relatively small, and the quantitation of 45Ca movements was corrected for this change. The addition of 1 microM Bay K 8644 to the perfusate stimulated tension and augmented Ca2+ depletion from the extracellular space. The addition of 15 microM nifedipine to the perfusate significantly reduced both tension development and Ca2+ depletion from the extracellular space of the muscle. Net contraction-dependent movement of Ca2+ from the extracellular space into the myocardium under control conditions at 1 mM [Ca2+] was 10-14 mumol Ca2+/kg tissue wet wt/beat. This value indicates either a large contribution of Ca2+-induced Ca2+ release from the sarcoplasmic reticulum and/or significant contribution of sarcolemmal bound Ca2+ to excitation-contraction coupling in the rabbit ventricle.
本研究的目的是检测肌肉收缩过程中Ca2+从细胞外空间进入心肌的运动情况。通过随时间收集流出液滴来测量兔右心室壁与含45Ca的灌注液的平衡情况。该实验方案在静息肌肉中进行,然后在15 - 20分钟后以相同方式重复,不同之处在于在收集期过半时刺激肌肉收缩。由此我们能够定量45Ca运动中依赖收缩的变化。在使用[58Co]EDTA作为细胞外空间标志物的对照实验中,我们观察到收缩改变了该空间的体积。细胞外空间的这种改变相对较小,并且针对此变化对45Ca运动的定量进行了校正。向灌注液中添加1 microM的Bay K 8644可刺激张力并增加细胞外空间的Ca2+消耗。向灌注液中添加15 microM的硝苯地平可显著降低肌肉细胞外空间的张力发展和Ca2+消耗。在1 mM [Ca2+]的对照条件下,Ca2+从细胞外空间向心肌的净收缩依赖性运动为10 - 14微摩尔Ca2+/千克组织湿重/搏动。该值表明要么肌浆网中Ca2+诱导的Ca2+释放起了很大作用,要么肌膜结合Ca2+对兔心室的兴奋 - 收缩偶联有显著贡献。