中文摘要：

本文旨在研究急性低温／再复温对大鼠心室肌膜电位和钾电流的影响。膜电位和膜电流分别在全细胞膜片钳的电压钳和电流钳模式下记录。当细胞外灌流液从25℃降低到4℃后，一过性外向电流（transient outward current，Ito）完全消失，膜电位为＋60mV时的稳态外向K^＋电流（sustained outward K^＋ current，Iss）和膜电位为-120mV时的内向整流K^＋电流（inward rectifier K^＋ current，Ik1）分别降低（48.5±14.1）％和（35.7±18.2）％，同时，膜电位绝对值降低。当细胞外灌流液从4℃再升高到36℃后，膜电位出现一过性超级化，然后恢复到静息电位水平；在58个细胞中，有36个细胞伴随复温出现ATP-敏感性K^＋（ATP-sensitive K^＋，KATP）通道的激活。再复温引起的上述变化可以被Na^＋／K^＋-ATP酶抑制剂哇巴因（100μmol／L）所抑制。再复温引起的KATP通道激活也能被蛋白激酶A抑制剂H-89（100μmol／L）所抑制。在细胞膜电位被钳制在0mV时，当细胞外灌流液温度从25℃降低到4℃后，细胞的体积没有发生明显改变，但当再复温引起KATP通道激活后，细胞很快发生皱缩，同时细胞内部出现许多折光较强的斑点。上述结果表明急性低温／再复温对大鼠心室肌膜电位和K^＋电流有明显影响，并提示KATP通道激活可能与心肌低温／再复温损伤有关。

英文摘要：

The effects of acute cooling/rewarming on cardiac K^＋ currents and membrane potential were investigated. Membrane potential and current were assessed with whole-cell patch-clamp technique in current-and voltage-clamp modes. When the temperature of bath solution was decreased from 25℃ to 4℃, the transient outward current （Ito） was completely abolished, the sustained outward K^＋ current （Iss） at ＋60 mV and the inward rectifier K^＋ current （IK1） at -120 mV were depressed by （48.5±14.1）% and （35.7±18.2）%, respectively, and the membrane potential became more positive. After the temperature of bath solution was raised from 4℃ to 36℃, the membrane potential exhibited a transient hyperpolarization and then was maintained at a stable level. In some myocytes （36 out of 58）, activation of the ATP-sensitive K^＋（KATP） channels after rewarming was observed. The rewarming-induced change in the membrane potential was inhibited by the Na^＋/K^＋ -ATPase inhibitor ouabain （100μmol/L）, and the rewarming-elicited activation of KATP channels was inhibited by the protein kinase A inhibitor H-89 （100 μmol/L）. Moreover, decrease of the temperature from 25℃ to 4 ℃ did not induce any significant change in cell volume when the cell membrane potential was clamped at 0 mV. However, significant cell shrinkage with spots was observed soon after rewarming-induced activation of KATP channels. These data demonstrate that acute cooling/rewarming has a profound influence on the membrane potential and K^＋ currents of ventricular myocytes, and suggest that activation of KATP channels may play a role in cardiac cooling/rewarming injury.