HUMAN MYOCARDIAL ADENOSINE-TRIPHOSPHATASE ACTIVITIES IN HEALTH AND HEART-FAILURE
HUMAN MYOCARDIAL ADENOSINE-TRIPHOSPHATASE ACTIVITIES IN HEALTH AND HEART-FAILURE
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DOI：
10.1016/0002-8703(88)90529-7
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发表时间：
1988-01-01
影响因子：
4.8
通讯作者：
WALLICK, ET
中科院分区：
文献类型：
--
作者：
UNVERFERTH, DV;LEE, SW;WALLICK, ET
本研究旨在确定：正常人和扩张型心肌病患者的心肌腺苷三磷酸酶（ATP酶）活性，以及ATP酶活性是否与年龄、心力衰竭的原因和严重程度以及洋地黄治疗有关。对32例受试者进行了肌内膜活检。6个结果正常。其他26例心室衰竭为特发性（n = 15）、家族性（n = 3）、酒精诱导（n = 5）或与阿霉素治疗相关（n = 3）。分析活检组织的总、线粒体、Na+-K+、Ca++和Mg++ ATP酶活性。总ATP酶和线粒体ATP酶活性与左心室射血分数相关（r分别= 0.65和0.67;均p = 0.0001）。残余Mg++ ATP酶活性与超声心动图测量的心室功能弱相关（p = 0.05）。在接受洋地黄治疗的患者中，Na+-K+ ATP酶活性受到抑制（p = 0.01）。这些结果表明，进行性心室功能障碍可能与总ATP酶，线粒体ATP酶，并在较小程度上，Mg++ ATP酶活性的进行性损失。虽然线粒体ATP酶活性降低不太可能是心室功能障碍的主要原因，但它可能通过导致三磷酸腺苷产生不足而使衰竭持续下去。对ATP酶活性的进一步研究可能为心力衰竭的发病机制提供更多的见解。
This study was designed to determine: the myocardial adenosine triphosphatase (ATPase) activities of normal humans and patients with dilated cardiomyopathy and whether ATPase activity is related to age, cause and severity of heart failure, and digitalis therapy. Endomyocardial biopsies were performed in 32 subjects. Results from six were normal. Ventricular failure in the other 26 was idiopathic (n = 15), familial (n = 3), alcohol induced (n = 5), or related to doxorubicin therapy (n = 3). The biopsies were analyzed for total, mitochondrial, Na+-K+, Ca++, and Mg++ ATPase activities. Total and mitochondrial ATPase activities correlated with left ventricular ejection fraction (r = 0.65 and 0.67, respectively; both p = 0.0001). Residual Mg++ ATPase activity correlated weakly with ventricular function as measured by echocardiography (p = 0.05). Na+-K+ ATPase activity was depressed in patients receiving digitalis (p = 0.01). These results suggest that progressive ventricular dysfunction may be associated with a progressive loss of total ATPase, mitochondrial ATPase and, to a lesser extent, Mg++ ATPase activity. Although depressed mitochondrial ATPase activity is not likely to be the primary cause of ventricular dysfunction, it could perpetuate failure by leading to inadequate production of adenosine triphosphate. Further study of ATPase activities may provide additional insight into the pathogenesis of cardiac failure.