Dhalla N S, Tomlinson C W, Singh J N, Lee S L, McNamara D B, Harrow J A, Yates J C
Recent Adv Stud Cardiac Struct Metab. 1976;9:377-94.
Sarcolemmal Ca++-ATPase, Mg++-ATPase, and (Na+-K+)-ATPase activities were increased in late stages of heart failure in myopathic hamsters (BIO 14.6) without any changes in the adenylate cyclase activity. On the other hand, these hamsters at early and moderate stages of heart failure showed depressions in mitochondrial calcium binding and uptake and microsomal calcium binding. Sarcolemmal (Na+-K+)-ATPase was decreased in failing hearts because of substrate lack, oxygen lack, and perfusion with Ca++-free, Na+-free, or K+-free medium. Both Mg++-ATPase and Ca++-ATPase activities of sarcolemma did not change on perfusing the hearts with substrate-free, hypoxic, Na+-free, or K+-free medium. Adenylate cyclase activity decreased on substrate-free or Ca++-free perfusion. Intracellular calcium overload produced by perfusing the hearts with medium containing calcium after Ca++-free perfusion was associated with decrease in all the sarcolemmal-bound enzyme activities. All types of failing hearts employed in this study showed a dramatic shift in the electrolyte composition. Failure of the cardiac muscle to generate contractile force on treatment with trypsin was associated with defects in the functions of sarcolemma, mitochondria, and sarcoplasmic reticulum, whereas such an effect on treatment with phospholipase C was limited to alterations in the activities of sarcolemma. The data suggest that abnormality at the level of sarcolemma plays an important role in the pathogenesis of heart dysfunction; however, the degree and direction of alterations in the sarcolemmal functions seem to be dependent upon the type of heart failure.
在患有心肌病的仓鼠（BIO 14.6）心力衰竭晚期，肌膜Ca++-ATP酶、Mg++-ATP酶和（Na+-K+）-ATP酶活性增加，而腺苷酸环化酶活性无任何变化。另一方面，这些处于心力衰竭早期和中期的仓鼠线粒体钙结合和摄取以及微粒体钙结合降低。由于底物缺乏、缺氧以及用无Ca++、无Na+或无K+的培养基灌注，衰竭心脏中的肌膜（Na+-K+）-ATP酶减少。用无底物、缺氧、无Na+或无K+的培养基灌注心脏时，肌膜的Mg++-ATP酶和Ca++-ATP酶活性均未改变。无底物或无Ca++灌注时，腺苷酸环化酶活性降低。在无Ca++灌注后用含钙培养基灌注心脏所产生的细胞内钙超载与所有肌膜结合酶活性降低有关。本研究中使用的所有类型的衰竭心脏均显示电解质组成发生了显著变化。用胰蛋白酶处理后心肌无法产生收缩力与肌膜、线粒体和肌浆网功能缺陷有关，而用磷脂酶C处理的这种作用仅限于肌膜活性的改变。数据表明，肌膜水平的异常在心脏功能障碍的发病机制中起重要作用；然而，肌膜功能改变的程度和方向似乎取决于心力衰竭的类型。
