培养大鼠心肌细胞缺氧与复氧时H~＋－Ca^（2＋）交换的研究

STUDY OF H￣+-Ca￣(2+)EXCHANGE IN CULTURED HEART CELLS AFTER HYPOXIA AND REOXYGENATION

大量研究表明：心肌细胞缺氧后再复氧，可因氧反常和ｐＨ反常造成细胞内Ｃａ２＋超载。通常认为，在心肌细胞发生ｐＨ反常后，Ｈ＋－Ｎａ＋和Ｎａ＋－Ｃａ２＋交换加强是细胞内Ｃａ２＋超载的重要机制。本实验结果表明：阻断了Ｈ＋－Ｎａ＋和Ｎａ＋－Ｃａ２＋交换后，仍有部分Ｃａ２＋进入细胞，Ｃａ２＋内流量与缺氧时间成正比关系。在无Ｎａ＋溶液中也得到了同样结果，表明此时Ｃａ２＋内流是通过与Ｎａ＋无关的通路进入细胞的。进一步实验表明这种Ｃａ２＋内流与细胞膜内外ｐＨ梯度差密切相关。当胞外ｐＨ升高即胞内相对Ｈ＋浓度增加时，Ｃａ２＋内流量也增加。故推测：ｐＨ反常所致细胞内Ｃａ２＋超载的原因，除Ｈ＋－Ｎａ＋和Ｎａ＋－Ｃａ２＋交换外，尚有Ｈ＋－Ｃａ２＋交换机制。

Reoxygenation is more serious for hypoxic myocardial cells because of the subscquence calcium overload. The calcium overload is known due to augmentation of H+-Na+, Na+-Ca2+, exchange during PH paradox. But the present experiment showedthat, when H+-Na+, Na+-Ca2+ exchange was inhibited, calcium could still enter myocardial cells after hypoxia or reoxygenation. Similar result was observed after usingNa+-Free solution, suggesting that calcium entance into the cell was unrelated to Na+channel. It was further shown that calcium accumulation was related to PH gradientacross the myocardial cell membrane, i. e., being increased with increase of H+ concentration in the cell. Therefore, it appears that, besides H+-Na+, Na+-Ca2+ exchange,H+-Ca2+ exchange is one of the reasens of calcium overload during intracellular pHparadox.