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首页> 外文期刊>American Journal of Physiology >Cardiac preconditioning with 4-h, 17 degrees C ischemia reduces (Ca(2+))(i) load and damage in part via K(ATP) channel opening.
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Cardiac preconditioning with 4-h, 17 degrees C ischemia reduces (Ca(2+))(i) load and damage in part via K(ATP) channel opening.

机译：进行4小时，17摄氏度局部缺血的心脏预处理可减少（Ca（2 +））（i）负荷，并部分通过K（ATP）通道打开而造成损伤。

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摘要

Brief ischemia before normothermic ischemia protects hearts against reperfusion injury (ischemic preconditioning, IPC), but it is unclear whether it protects against long-term moderate hypothermic ischemia. We explored in isolated guinea pig hearts 1) the influence of two 2-min periods of normothermic ischemia before 4 h, 17 degrees C hypothermic ischemia on cardiac cytosolic [Ca(2+)], mechanical and metabolic function, and infarct size, and 2) the potential role of K(ATP) channels in eliciting cardioprotection. We found that IPC before 4 h moderate hypothermia improved myocardial perfusion, contractility, and relaxation during normothermic reperfusion. Protection was associated with markedly reduced diastolic [Ca(2+)] loading throughout both hypothermic storage and reperfusion. Global infarct size was markedly reduced from 36 +/- 2 (SE)% to 15 +/- 1% with IPC. Bracketing ischemic pulses with 200 microM 5-hydroxydecanoic acid or 10 microM glibenclamide increased infarct size to 28 +/- 3% and 26 +/- 4%,respectively. These results suggest that brief ischemia before long-term hypothermic storage adds to the cardioprotective effects of hypothermia and that this is associated with decreased cytosolic [Ca(2+)] loading and enhanced ATP-sensitive K channel opening.
机译：常温缺血之前的短暂缺血可保护心脏免受再灌注损伤（缺血预处理，IPC），但尚不清楚它是否可预防长期的中度低温缺血。我们在离体的豚鼠心脏中进行了探索：1）在4小时，17°C的低温缺血之前，两个2分钟的常温缺血对心脏胞质[Ca（2+）]，机械和代谢功能以及梗死面积的影响，以及2）K（ATP）通道在引发心脏保护中的潜在作用。我们发现中度低温4小时之前的IPC改善了常温再灌注过程中的心肌灌注，收缩力和松弛。在整个低温保存和再灌注过程中，保护与舒张压[Ca（2+）]负荷显着降低有关。使用IPC，全球梗塞面积从36 +/- 2（SE）％显着降低到15 +/- 1％。用200 microM 5-羟基癸酸或10 microM格列本脲进行的支架缺血脉冲将梗塞面积分别增加至28 +/- 3％和26 +/- 4％。这些结果表明长期低温存储之前短暂的缺血增加了低温的心脏保护作用，并且这与减少的胞质[Ca（2+）]负载和增强的ATP敏感性K通道开放有关。

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