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首页> 外文期刊>Life sciences >ATP-dependent potassium channels involved in the cardiac protection induced by intermittent hypoxia against ischemia/reperfusion injury.
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ATP-dependent potassium channels involved in the cardiac protection induced by intermittent hypoxia against ischemia/reperfusion injury.

机译：ATP依赖性钾离子通道参与了针对缺血/再灌注损伤的间歇性低氧所致的心脏保护。

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The aim of this study was to investigate the protection afforded by intermittent hypoxia (IH) against ischemia/reperfusion injury and its effects on calcium homeostasis during ischemia/reperfusion. The roles of KATP channels in these two actions were to be explored. Isolated hearts from IH and normoxic rats were subjected to 30 min global ischemia followed by 30 min reperfusion. Cardiac function was less deteriorated during ischemia and reperfusion in the IH rat hearts compared to normoxia rat hearts. Amplitude of the maximal contracture during ischemia was lower, while time to maximal contracture was extended in IH hearts. Post-ischemic recovery of left ventricular developed pressure and +/-dP/dtmax were higher in IH hearts than in normoxic hearts. KATP antagonist glibenclamide (10 microM) completely abolished these protective effects of IH, but had no appreciable influence on normoxic hearts. In cardiomyocytes isolated from normoxic hearts, [Ca2+]i, measured as arbitrary units of fluorescence ratio (340 nm/380 nm) of fura-2, gradually increased during 20 min simulated ischemia and kept at high level during 30 min reperfusion (1.081 +/- 0.004 and 1.088 +/- 0.006 respectively, p<0.01 vs pre-ischemia perfusion). However, in cardiomyocytes isolated from IH hearts, [Ca2+]i kept at normal level during ischemia and reperfusion (1.012 +/- 0.006 and 1.021 +/- 0.002 respectively, P>0.05 vs pre-ischemia perfusion). 10 microM glibenclamide and 100 microM 5-hydroxydecanoate (a selective mitochondria KATP antagonist) respectively abolished this effect of IH; calcium overloading reappeared during ischemia (1.133 +/- 0.007 and 1.118 +/- 0.007 respectively, P<0.01) and reperfusion (1.091 +/- 0.004 and 1.095 +/- 0.012 respectivly, P<0.01). However they had no effects on simulated ischemia and reperfusion-induced calcium overloading in normoxic myocytes. 50 microM pinacidil, a KATP opener, attenuated calcium overloading during ischemia and reperfusion in normoxic myocytes, but had no effect on [Ca2+]i change in IH myocytes. These results suggested that KATP channels contributed to the cardiac protection induced by IH against ischemia/reperfusion injury; the elimination of calcium overloading during ischemia/reperfusion by IH might underlie the mechanism of protection.
机译：这项研究的目的是研究间歇性缺氧（IH）对缺血/再灌注损伤的保护作用及其对缺血/再灌注过程中钙稳态的影响。将探讨KATP通道在这两个动作中的作用。将来自IH和常氧大鼠的离体心脏进行30分钟的整体缺血，然后再进行30分钟的再灌注。与正常氧大鼠心脏相比，IH大鼠心脏的心脏功能在缺血和再灌注期间的恶化程度较小。缺血期间最大挛缩的幅度较低，而IH心脏中最大挛缩的时间延长。 IH心脏缺血性恢复后左心室发育压力和+/- dP / dtmax高于常氧性心脏。 KATP拮抗剂格列本脲（10 microM）完全取消了IH的这些保护作用，但对常氧心脏没有明显影响。在从常氧心脏分离的心肌细胞中，[Ca2 +] i（以fura-2的荧光比（340 nm / 380 nm）的任意单位测量）在模拟缺血20分钟内逐渐增加，并在30分钟再灌注过程中保持高水平（1.081 +分别为0.004和1.088 +/- 0.006，与缺血前灌注相比p <0.01）。然而，在从IH心脏分离的心肌细胞中，[Ca2 +] i在缺血和再灌注期间保持正常水平（分别为1.012 +/- 0.006和1.021 +/- 0.002，与缺血前灌注相比，P> 0.05）。 10 microM格列本脲和100 microM 5-羟基癸酸酯（一种选择性的线粒体KATP拮抗剂）消除了IH的这种作用;缺血期间（分别为1.133 +/- 0.007和1.118 +/- 0.007，P <0.01）和再灌注（分别为1.091 +/- 0.004和1.095 +/- 0.012，P <0.01）再次出现钙超载。然而，它们对常氧肌细胞中的模拟缺血和再灌注诱导的钙超载没有影响。 50 microM吡那地尔，一种KATP开启剂，可减轻常氧性心肌细胞在缺血和再灌注过程中的钙超载，但对IH心肌细胞中[Ca2 +] i的变化没有影响。这些结果表明，KATP通道有助于IH诱导的心肌缺血/再灌注损伤的保护作用。 IH消除缺血/再灌注时钙超载可能是其保护机制的基础。

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