Kim M J, Park S R, Suh C K
Department of Physiology, Inha University College of Medicine, Inchon Korea.
Yonsei Med J. 1993 Jun;34(2):133-44. doi: 10.3349/ymj.1993.34.2.133.
The removal of Ca2+ from the cardioplegic solutions could cause the danger of inducing a "calcium paradox" during reperfusion. Since intracellular Ca2+ activities are coupled to Na+ activities via Na(+)-Ca2+ exchange, an increase in intracellular Na+ activities during the cardioplegia could cause an abrupt Ca2+ influx when reperfused. To study the effects of Na+ and Ca2+ concentrations in cardioplegic solutions on intracellular Ca2+ activities during the cardioplegia and subsequent recovery period, the membrane potential and intracellular Na+ and Ca2+ activities of guinea pig ventricular papillary were measured. 1) A cardioplegia with low Ca2+ cardioplegic solution significantly decreased the overshoot and duration of the first action potential after cardioplegia, but the changes in action potential configuration were minimized after a cardioplegia with Ca2+ concentration adjusted according to the Na(+)-Ca2+ exchange mechanism. 2) Intracellular Na+ activity was continuously decreased during the cardioplegia, and the intracellular Na+ activity 20 minutes after cardioplegia was the highest with low Ca2+ cardioplegic solution. 3) Intracellular Na+ and Ca2+ activities were continuously decreased during the cardioplegia with Ca2+ concentration adjusted according to the Na(+)-Ca2+ exchange mechanism. 4) During a reperfusion of Tyrode solution after cardioplegia intracellular Na+ and Ca2+ activities were increased. Intracellular Ca2+ activity was increased more rapidly than intracellular Na+ activity. 5) The rate of increase in intracellular Ca2+ activity with reperfusion of Tyrode solution was dependent upon intracellular Na+ activity during cardioplegia, in such a way that the higher the intracellular Na+ activity was, the faster the intracellular Ca2+ activity increased. These data suggest that Na(+)-Ca2+ exchange mechanism may play an important role in the regulation of intracellular Ca2+ activity during recovery after cardioplegia.
从心脏停搏液中去除Ca2+可能会在再灌注期间引发“钙反常”的危险。由于细胞内Ca2+活性通过Na(+)-Ca2+交换与Na+活性相耦联，心脏停搏期间细胞内Na+活性的增加在再灌注时可能会导致Ca2+突然内流。为了研究心脏停搏液中Na+和Ca2+浓度对心脏停搏期间及随后恢复期细胞内Ca2+活性的影响，测量了豚鼠心室乳头肌的膜电位以及细胞内Na+和Ca2+活性。1）使用低Ca2+心脏停搏液进行心脏停搏可显著降低心脏停搏后第一个动作电位的超射值和持续时间，但根据Na(+)-Ca2+交换机制调整Ca2+浓度的心脏停搏后，动作电位形态的变化最小。2）在心脏停搏期间，细胞内Na+活性持续降低，使用低Ca2+心脏停搏液时，心脏停搏20分钟后的细胞内Na+活性最高。3）根据Na(+)-Ca2+交换机制调整Ca2+浓度的心脏停搏期间，细胞内Na+和Ca2+活性持续降低。4）心脏停搏后用台氏液再灌注期间，细胞内Na+和Ca2+活性增加。细胞内Ca2+活性比细胞内Na+活性增加得更快。5）用台氏液再灌注时细胞内Ca2+活性的增加速率取决于心脏停搏期间的细胞内Na+活性，即细胞内Na+活性越高，细胞内Ca2+活性增加得越快。这些数据表明，Na(+)-Ca2+交换机制可能在心脏停搏后恢复期间细胞内Ca2+活性的调节中起重要作用。
