Intracellular Calcium and Myocardial Contractility: III. Reduced Calcium Uptake and Atpase of the Sarcoplasmic Reticular Fraction Prepared from Chronically Failing Calf Hearts
Intracellular Calcium and Myocardial Contractility: III. Reduced Calcium Uptake and Atpase of the Sarcoplasmic Reticular Fraction Prepared from Chronically Failing Calf Hearts
复制标题
细胞内钙和心肌收缩力：III。
作者：
J. Suko;J. Vogel;C. Chidsey
通过比较从对照小牛和实验诱导肺动脉高压期间发生右心室衰竭的小牛心脏制备的微粒体中的钙摄取和钙激活ATP酶，在体外研究了衰竭心肌的肌浆网功能。在25°C下，在草酸盐存在下，对照制剂中钙摄取率平均为0.147 μ mol·mg−1·min−1，而在右心室衰竭的制剂中钙摄取率显著降低（平均0.086 μ mol·mg−1·min−1）。失败时钙激活ATP酶也显著减少（平均值为0.184，而0.073 μ mol·mg−1·min−1）。虽然两种制剂也显示出减少的钙活动，在非衰竭的左心室，这些活动并没有显着的抑制，从小牛心室的制剂失败。在37°C下观察到通过蔗糖梯度离心进一步纯化的制剂的钙活性的类似降低。在不存在草酸盐的情况下，微粒体的摄取能力（测量为钙摄取）在衰竭心脏的制剂中没有减少。线粒体污染似乎并不是一个因素，因为叠氮化物几乎完全抑制线粒体中的钙活性，而在对照组和衰竭心脏的微粒体中，抑制作用均小于10%。哇巴因对衰竭心脏的微粒体没有影响。这些研究表明，有一个缺陷，在微粒体中的钙转运和心肌细胞的肌浆网的功能异常，在完整的心力衰竭，可能会导致临床上重要的兴奋-收缩偶联机制的变化。
The function of the sarcoplasmic reticulum of the failing myocardiums was studied in vitro by comparing calcium uptake and calcium-activated ATPase in microsomes prepared from hearts of control calves and calves in which right ventricular failure developed during experimentally induced pulmonary hypertension. The rate of calcium uptake averaged .147 μmole·mg−1·min−1 at 25°C in the presence of oxalate in control preparations and was significantly reduced in preparations from failing right ventricles (avg .086 μmoles·mg−1·min−1). Calcium-activated ATPase was also diminished significantly in failure (avg .184 compared to .073 μmoles·mg−1·min−1). Although two preparations also showed diminished calcium activities in the nonfailing left ventricle, group these activities were not significantly depressed in preparations from ventricle in calves with failure. A similar reduction in calcium activities observed at 37°C with preparations further purified by sucrose gradient centrifugation. The uptake capacity of microsomes, measured as calcium uptake in the absence of oxalate, was not diminished in the preparations from failing hearts. Mitochondrial contamination did not appear to be a factor since azide inhibited calcium activity almost completely in mitochondria, whereas inhibition was less than 10% in microsomes of both control and failing hearts. Ouabain had no effect on the microsomes from failing hearts. These studies indicate that there is a defect in calcium transport in microsomes and a functional abnormality of the sarcoplasmic reticulum in the intact myocardial cell in heart failure which could lead to changes in the excitation-contraction coupling mechanisms of clinical importance.