Carvedilol inhibits mitochondrial oxygen consumption and superoxide production during calcium overload in isolated heart mitochondria

Carvedilol inhibits mitochondrial oxygen consumption and superoxide production during calcium overload in isolated heart mitochondria
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DOI:
10.1253/circj.70.321
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发表时间:
2006-03-01
影响因子:
3.3
通讯作者:
Matsuzaki, M
Matsuzaki, M
中科院分区:
医学3区
文献类型:
--
作者:
Kametani, R;Miura, T;Matsuzaki, M

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背景彗星研究提示卡维地洛治疗心力衰竭的疗效优于美托洛尔。然而,其潜在的行动机制仍不清楚。方法测定大鼠心肌线粒体耗氧量(MVO(2))和线粒体ROS生成量。Ca~(2+)超载从10~100Mol/m o l/L增加MVO(2)由527+/-139增加到671+/-138mnol/mg(p
Background The COMET study suggested the better effect of carvedilol to metoprolol in treating heart failure. However, its underlying mechanisms of action remain unclear. As a result, evaluation of the distinct effects of both drugs oil the mitochondrial function and reactive oxygen species (ROS) production during Ca2+ overload was investigated.Methods and Results The mitochondrial oxygen consumption (mVO(2)) and the mitochondrial ROS production in isolated rat heart mitochondria was measured. Ca2+ overload from 10 to 100/mu mol/L augmented mVO(2) was from 527 +/- 139 to 671 +/- 138 mnol/mg (p