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首页> 外文期刊>American Journal of Physiology >Protective effect of gap junction uncouplers given during hypoxia against reoxygenation injury in isolated rat hearts.
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Protective effect of gap junction uncouplers given during hypoxia against reoxygenation injury in isolated rat hearts.

机译：缺氧时给予的间隙连接解偶联剂对离体大鼠心脏的复氧损伤的保护作用。

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摘要

It has been shown that cell-to-cell chemical coupling may persist during severe myocardial hypoxia or ischemia. We aimed to analyze the effects of different, chemically unrelated gap junction uncouplers on the progression of ischemic injury in hypoxic myocardium. First, we analyzed the effects of heptanol, 18alpha-glycyrrhetinic acid, and palmitoleic acid on intracellular Ca2+ concentration during simulated hypoxia (2 mM NaCN) in isolated cardiomyocytes. Next, we analyzed their effects on developed and diastolic tension and electrical impedance in 47 isolated rat hearts submitted to 40 min of hypoxia and reoxygenation. All treatments were applied only during the hypoxic period. Cell injury was determined by lactate dehydrogenase (LDH) release. Heptanol, but not 18alpha-glycyrrhetinic acid nor palmitoleic acid, attenuated the increase in cytosolic Ca2+ concentration induced by simulated ischemia in cardiomyocytes and delayed rigor development (rigor onset at 7.31 +/- 0.71 min in controls vs. 14.76 +/- 1.44 in heptanol-treated hearts, P < 0.001) and the onset of the marked changes in electrical impedance (tissue resistivity: 4.02 +/- 0.29 vs. 7.75 +/- 1.84 min, P = 0.016) in hypoxic rat hearts. LDH release from hypoxic hearts was minimal and was not significantly modified by drugs. However, all gap junction uncouplers, given during hypoxia, attenuated LDH release during subsequent reoxygenation. Dose-response analysis showed that increasing heptanol concentration beyond the level associated with maximal effects on cell coupling resulted in further protection against hypoxic injury. In conclusion, gap junction uncoupling during hypoxia has a protective effect on cell death occurring upon subsequent reoxygenation, and heptanol has, in addition, a marked protective effect independent of its uncoupling actions.
机译：已经显示在严重的心肌缺氧或局部缺血期间细胞间化学偶联可能持续。我们旨在分析不同的化学无关的间隙连接解偶联剂对缺氧心肌缺血性损伤进展的影响。首先，我们分析了在孤立的心肌细胞模拟缺氧（2 mM NaCN）过程中庚醇，18α-甘草次酸和棕榈油酸对细胞内Ca2 +浓度的影响。接下来，我们在40分钟缺氧和复氧的情况下，分析了它们对47只离体大鼠心脏发达和舒张张力和电阻抗的影响。所有治疗仅在缺氧期进行。细胞损伤通过乳酸脱氢酶（LDH）释放来确定。庚醇而不是18α-甘草次酸或棕榈油酸可减轻心肌细胞模拟缺血诱导的胞浆Ca2 +浓度增加，并延缓严峻的发育（对照组中的起始于7.31 +/- 0.71分钟，庚烷中的起始于14.76 +/- 1.44。处理过的心脏，P <0.001）和低氧大鼠心脏电阻抗的显着变化（组织电阻率：4.02 +/- 0.29 vs. 7.75 +/- 1.84 min，P = 0.016）。缺氧心脏中的LDH释放极少，并且没有被药物明显修饰。然而，在缺氧期间给予的所有间隙连接解偶联剂在随后的复氧期间减弱了LDH的释放。剂量反应分析表明，庚醇浓度的增加超过与对细胞偶联的最大影响相关的水平，可进一步抵抗缺氧损伤。总之，缺氧期间的间隙连接解偶联对随后的复氧反应中发生的细胞死亡具有保护作用，此外，庚醇还具有显着的保护作用，而与其解偶联作用无关。

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