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The cytoplasmic phosphorylation potential. Its possible role in the control of myocardial respiration and cardiac contractility.

作者信息

Gibbs C

出版信息

J Mol Cell Cardiol. 1985 Aug;17(8):727-31. doi: 10.1016/s0022-2828(85)80034-1.

DOI:10.1016/s0022-2828(85)80034-1
PMID:3900424
Abstract
摘要

相似文献

1
The cytoplasmic phosphorylation potential. Its possible role in the control of myocardial respiration and cardiac contractility.
J Mol Cell Cardiol. 1985 Aug;17(8):727-31. doi: 10.1016/s0022-2828(85)80034-1.
2
Control of respiration by the mitochondrial phosphorylation state.线粒体磷酸化状态对呼吸的控制。
Arch Biochem Biophys. 1974 Apr 2;161(2):581-91. doi: 10.1016/0003-9861(74)90341-5.
3
Effect of graded reductions of coronary pressure and flow on myocardial metabolism and performance: a model of "hibernating" myocardium.冠状动脉压力和流量分级降低对心肌代谢及功能的影响:“冬眠”心肌模型
J Am Coll Cardiol. 1991 Jun;17(7):1661-70. doi: 10.1016/0735-1097(91)90662-s.
4
[Cardiac functions].[心脏功能]
Nihon Seirigaku Zasshi. 2003;65(7-8):204-16.
5
Cardiac energetics.心脏能量学
Physiol Rev. 1978 Jan;58(1):174-254. doi: 10.1152/physrev.1978.58.1.174.
6
Mitochondrial NADH in the Langendorff rat heart decreases in response to increases in work: increase of cardiac work is associated with decrease of mitochondrial NADH.在离体灌流的大鼠心脏中,线粒体烟酰胺腺嘌呤二核苷酸(NADH)会随着心脏做功的增加而减少:心脏做功的增加与线粒体NADH的减少相关。
Adv Exp Med Biol. 1996;388:275-82. doi: 10.1007/978-1-4613-0333-6_35.
7
The mechanism of respiratory control in the in vivo heart.体内心脏的呼吸控制机制。
J Mol Cell Cardiol. 1989 Feb;21 Suppl 1:59-66. doi: 10.1016/0022-2828(89)90838-9.
8
The interpretation of experimentally obtained values of the cytoplasmic phosphorylation potential.实验获得的细胞质磷酸化电位值的解读。
J Mol Cell Cardiol. 1988 Dec;20(12):1203-9. doi: 10.1016/0022-2828(88)90599-8.
9
[Contractile function and energy metabolism of the myocardium during emotional stress and adaptation of animals to brief exposure to stress].[情绪应激及动物对短暂应激适应过程中心肌的收缩功能与能量代谢]
Fiziol Zh SSSR Im I M Sechenova. 1986 May;72(5):632-6.
10
[Depletion of cytoplasmic ATP in the heart and the contractile function of the myocardium].[心脏细胞质ATP的消耗与心肌的收缩功能]
Dokl Akad Nauk SSSR. 1986;291(2):483-7.

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NADH changes during hypoxia, ischemia, and increased work differ between isolated heart preparations.在缺氧、缺血和工作增加期间,NADH 的变化在分离的心脏制剂之间有所不同。
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Creatine kinase adenosine triphosphate and phosphocreatine energy supply in a single kindred of patients with hypertrophic cardiomyopathy.肌酸激酶三磷酸腺苷和磷酸肌酸能量供应在一个家族性肥厚型心肌病患者。
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Creatine kinase overexpression improves ATP kinetics and contractile function in postischemic myocardium.肌酸激酶过表达改善缺血后心肌的 ATP 动力学和收缩功能。
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