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首页> 外文期刊>Bulletin of experimental biology and medicine >Role of ATP-sensitive K(+)-channels in antiarrhythmic and cardioprotective action of adaptation to intermittent hypobaric hypoxia.
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Role of ATP-sensitive K(+)-channels in antiarrhythmic and cardioprotective action of adaptation to intermittent hypobaric hypoxia.

机译:ATP敏感性K(+)通道在适应间歇性低压低氧的抗心律不齐和心脏保护作用中的作用。

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Mature Wistar rats were exposed to intermittent hypobaric hypoxia (5000 m, 6 h/day, 30 sessions). This mode of adaptation enhanced heart tolerance to the arrhythmogenic action of 45-min coronary occlusion, but does not affect the infarction size/risk area ratio. In some series, the rats were exposed to more severe intermittent hypobaric hypoxia (7000 m, 8 h/day, 6 weeks) followed by 20-min coronary occlusion and 3-h reperfusion one day after the last hypoxia session. In this case, adaptation reduced the infarction size/risk area ratio and enhanced cardiac tolerance to the arrhythmogenic effect of reperfusion, but had no effect on the incidence of ventricular arrhythmia during ischemia. We found that the cardioprotective and antiarrhythmic effects of adaptation to an altitude of 7000 m and the antiarrhythmic effect of 5000-m adaptation were mediated via activation of K(ATP) channels.
机译:成熟的Wistar大鼠暴露于间歇性低压缺氧(5000 m,6小时/天,30个疗程)。这种适应模式增强了对45分钟冠状动脉闭塞的心律失常作用的心脏耐受性,但不影响梗死面积/风险面积比。在某些系列中,大鼠在最后一次低氧疗程后的一天暴露于更严重的间歇性低压缺氧(7000 m,每天8小时,每天6周),然后进行20分钟的冠状动脉闭塞和3小时的再灌注。在这种情况下,适应降低了梗塞面积/风险面积比,增强了对再灌注致心律失常作用的心脏耐受性,但对缺血期间室性心律失常的发生率没有影响。我们发现适应海拔7000 m的心脏保护和抗心律不齐的作用以及适应5000 m的抗心律不齐的作用是通过激活K(ATP)通道介导的。

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