Increased inducible nitric oxide synthase in skeletal muscle biopsies from patients with chronic heart failure
Increased inducible nitric oxide synthase in skeletal muscle biopsies from patients with chronic heart failure
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DOI：
10.1006/bmme.1997.2598
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发表时间：
1997-08-01
期刊：
影响因子：
--
通讯作者：
Hambrecht, R
中科院分区：
文献类型：
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作者：
Adams, V;Yu, JT;Hambrecht, R
除了左心室泵衰竭和低心输出量外，骨骼肌的结构和代谢改变被认为是CHF患者运动不耐受的原因。使用心肌细胞的研究表明，由诱导型一氧化氮合酶（iNOS）产生的一氧化氮可能与扩张型心肌病的发生有关。本研究旨在确定充血性心力衰竭患者工作骨骼肌中的iNOS。用特异性抗体通过免疫组化检测骨骼肌活检组织中的iNOS（m.股外侧肌）的肌电图。这种表达仅限于骨骼肌细胞，在慢性心力衰竭患者中增加了5 - 9倍。扩张型心肌病与缺血型心肌病患者iNOS表达差异无统计学意义。局部iNOS表达增加的发现和NO减弱骨骼肌收缩性能的实验证据表明，iNOS的表达可能是慢性心力衰竭患者运动不耐受的原因。(C)1997年学术出版社。
In addition to left ventricular pump failure and low cardiac output, structural and metabolic alterations of skeletal muscle are thought to contribute to exercise intolerance seen in patients with CHF. Studies using cardiac myocytes have implicated nitric oxide elaborated by inducible nitric oxide synthase (iNOS) as a potential agent associated with the genesis of dilated cardiomyopathy. The present study was designed to locate iNOS in the working skeletal muscle of patients with congestive heart failure. Specific antibodies were used to detect iNOS by immunohistochemistry in skeletal muscle biopsies (m. vastus lateralis) of 37 patients with left ventricular pump failure and 8 normal controls. The expression was restricted to skeletal muscle myocytes and was increased five-to ninefold in patients with chronic heart failure. There was no statistically significant difference in iNOS expression between patients with dilated cardiomyopathy and those with ischemic cardiomyopathy. The finding of a locally increased expression of iNOS and the experimental evidence that NO attenuates the contractile performance of the skeletal muscle suggest that the expression of iNOS may be responsible for the exercise intolerance seen in patients with chronic heart failure. (C) 1997 Academic Press.