Activation of NADPH oxidase during progression of cardiac hypertrophy to failure
Activation of NADPH oxidase during progression of cardiac hypertrophy to failure
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DOI：
10.1161/01.hyp.0000032031.30374.32
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发表时间：
2002-10-01
期刊：
影响因子：
8.3
通讯作者：
Shah, AM
中科院分区：
文献类型：
--
作者：
Li, JM;Gall, NP;Shah, AM
活性氧（ROS）产生增加与左心室（LV）肥大和心力衰竭的病理生理学有关。然而，心肌ROS产生的酶源尚不清楚。我们研究了吞噬型NADPH氧化酶在实验性豚鼠进行性压力超负荷左室肥厚模型的左室心肌中的表达和活性。伴随着左心室肥大的发展，通过光泽精（5 μ mol/L）化学发光或细胞色素c还原测定，左心室匀浆中NADPH依赖性O-2（-）的产生显著且进行性增加（在左心室失代偿阶段增加约40%; P
Increased reactive oxygen species (ROS) production is implicated in the pathophysiology of left ventricular (LV) hypertrophy and heart failure. However, the enzymatic sources of myocardial ROS production are unclear. We examined the expression and activity of phagocyte-type NADPH oxidase in LV myocardium in an experimental guinea pig model of progressive pressure-overload LV hypertrophy. Concomitant with the development of LV hypertrophy, NADPH-dependent O-2(-) production in LV homogenates, measured by lucigenin (5 mumol/L) chemiluminescence or cytochrome c reduction assays, significantly and progressively increased (by approximate to40% at the stage of LV decompensation; P