Pagani E D, Alousi A A, Grant A M, Older T M, Dziuban S W, Allen P D
Molecular Cardiology Unit, Sterling-Winthrop Research Institute, Rensselaer, New York 12144.
Circ Res. 1988 Aug;63(2):380-5. doi: 10.1161/01.res.63.2.380.
Force development and shortening by cardiac muscle occur as a result of the interaction between actin and myosin within the myofibrillar lattice. This interaction is dependent upon intracellular ionized calcium and is controlled by the troponin-tropomyosin regulatory proteins situated along the actin filament. In this study, we compared the myofibrillar content and myofibrillar Mg-ATPase activity of normal human ventricular muscle with that of ventricular muscle from patients in end-stage failure caused by coronary artery disease or cardiomyopathy and ventricular muscle from patients with heart failure due to mitral valve insufficiency. The results show that the amount of myofibrillar protein (mg/g wet wt ventricle) in hearts in end-stage failure (coronary artery disease and cardiomyopathy) is significantly lower compared with normal hearts and hearts in failure due to mitral valve insufficiency. However, the Mg-ATPase activity of myofibrils from hearts in both end-stage failure and failure due to mitral valve insufficiency is significantly lower compared with myofibrils from normal hearts. The data suggest that the reduction in the amount of myofibrillar protein in ventricular tissue is a pivotal event that may be responsible for the progression of heart disease to the point of end-stage failure.
心肌的力量产生和缩短是由于肌原纤维晶格中肌动蛋白和肌球蛋白之间的相互作用所致。这种相互作用依赖于细胞内的游离钙，并受沿肌动蛋白丝排列的肌钙蛋白 - 原肌球蛋白调节蛋白的控制。在本研究中，我们比较了正常人心室肌与冠状动脉疾病或心肌病所致终末期心力衰竭患者的心室肌以及二尖瓣关闭不全所致心力衰竭患者的心室肌的肌原纤维含量和肌原纤维Mg - ATP酶活性。结果表明，终末期心力衰竭（冠状动脉疾病和心肌病）患者心脏中的肌原纤维蛋白量（mg/g湿重心室）与正常心脏以及二尖瓣关闭不全所致心力衰竭患者的心脏相比显著降低。然而，终末期心力衰竭患者和二尖瓣关闭不全所致心力衰竭患者心脏的肌原纤维Mg - ATP酶活性与正常心脏的肌原纤维相比均显著降低。数据表明，心室组织中肌原纤维蛋白量的减少是一个关键事件，可能是心脏病发展至终末期心力衰竭的原因。
