MYOFIBRILLAR ADENOSINE TRIPHOSPHATASE ACTIVITY IN CONGESTIVE HEART FAILURE
MYOFIBRILLAR ADENOSINE TRIPHOSPHATASE ACTIVITY IN CONGESTIVE HEART FAILURE
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DOI：
10.1152/ajplegacy.1962.202.5.940
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发表时间：
1962-01-01
影响因子：
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通讯作者：
GORDON, MS
中科院分区：
文献类型：
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作者：
ALPERT, NR;GORDON, MS
本文研究了7个衰竭心脏和9个对照心脏的肌原纤维三磷酸腺苷酶（ATPase）活性。衰竭的心脏来自于良性原发性高血压后充血性心力衰竭的临床和病理诊断。正常的心脏是在创伤性死亡后获得的，在其他方面正常的受试者中没有病理学证据。随着MgCl_2浓度的增加，衰竭心肌肌原纤维ATP酶活性的升高幅度明显低于正常心肌。将底物浓度增加至5 mM三磷酸腺苷（ATP），正常组的肌原纤维ATP酶活性增加至最佳值0.95 [mu]M/mg/15 min，失败组的最佳值为0.69/[mu]M/mg/15 min。底物浓度的进一步增加降低了两组的ATP酶活性。结论是，良性原发性高血压后充血性心力衰竭心脏的肌原纤维水解ATP的速度比正常心脏慢。由于肌原纤维ATP酶活性和张力的发展密切相关，衰竭心脏ATP酶活性的降低可能是其无法满足工作负荷的原因，因此这些实验提供了证据，表明充血性心力衰竭的损害可能存在于收缩蛋白本身。
Myofibrillar adenosine triphosphatase (ATPase) activity from seven failing and nine control hearts was studied. The failing hearts came from patients with a clinical and pathological diagnosis of congestive heart failure following benign essential hypertension. Normal hearts were obtained following traumatic death in otherwise normal subjects with no evidence of pathology. As the MgCl2 concentra-tion was increased, the myofibrillar ATPase from the failing hearts exhibited a significantly lower rise in activity than that from the normal hearts. Increasing the substrate concentration to 5 mM adenosine triphosphate (ATP) increased the myofibrillar ATPase activity to an optimum of .95 [mu]M/mg/15 min in the normal group and .69/[mu]M/mg/15 min in the failing group. Further increases in substrate concentration decreased the ATPase activity in both groups. It was concluded that myofibrils from a heart in congestive failure following benign essential hypertension hydrolyze ATP at a slower rate than those from normal hearts. Since myofibrillar ATPase activity and tension development go hand in hand, the decrease in ATPase activity in the failing heart may account for its inability to meet the work load imposed upon it. Thus these experiments offer evidence that a lesion in congestive heart failure may reside in the contractile protein itself.