Selective effects of oxygen free radicals on excitation-contraction coupling in ventricular muscle - Implications for the mechanism of stunned myocardium
Selective effects of oxygen free radicals on excitation-contraction coupling in ventricular muscle - Implications for the mechanism of stunned myocardium
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DOI：
10.1161/01.cir.94.10.2597
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发表时间：
1996-11-15
期刊：
影响因子：
37.8
通讯作者：
Marban, E
中科院分区：
文献类型：
--
作者：
Gao, WD;Liu, YG;Marban, E
氧自由基（OFRs）与心肌休克的发病机制有关，但OFRs促进心肌休克的确切机制尚不清楚。我们研究了ofr直接暴露于心肌后发生的收缩功能障碍的病理生理，并将结果与休克心肌的病理生理进行了比较。方法与结果用fura-2离子负载大鼠右心室小梁，测定[Ca2+](i)。在ryanodine存在下，通过快速电刺激获得稳态力-[Ca2+](i)关系。采用H2O2+Fe3+-硝基三乙酸（H2O2+Fe3+）体系生成羟基自由基，黄嘌呤氧化酶+嘌呤（XO+P）体系生成超氧化物。在暴露于H2O2+Fe3+ 10分钟的肌肉中，抽搐力和Ca2+瞬态都降低了(例如，在1.5 mmol/L的外部[Ca2+]中，力从41+/-7降低到23+/-4 mN/mm(2)
Background Oxygen free radicals (OFRs) have been implicated in the pathogenesis of myocardial stunning, but the precise mechanism by which OFRs foster stunning remains unclear. We investigated the pathophysiology of the contractile dysfunction that occurs after direct exposure of OFRs to cardiac muscle and compared the results with the pathophysiology of stunned myocardium.Methods and Results Trabeculae from the right ventricles of rat hearts were loaded iontophoretically with fura-2 to determine [Ca2+](i). Steady-state force-[Ca2+](i) relations were obtained by rapid electrical stimulation in the presence of ryanodine. Two exogenous OFR-generating systems were used: H2O2+Fe3+-nitrilotriacetic acid (H2O2+Fe3+) to produce hydroxyl radical, and xanthine oxidase+purine (XO+P) to produce superoxide. In muscles exposed to H2O2+Fe3+ for 10 minutes, both twitch force and Ca2+ transients were decreased (eg, in 1.5 mmol/L external [Ca2+], force decreased from 41+/-7 to 23+/-4 mN/mm(2), P