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缺钾挛缩期间心肌中标记钙摄取的增加。

Increase of labeled calcium uptake in heart muscle during potassium lack contracture.

作者信息

THOMAS L J

出版信息

J Gen Physiol. 1960 Jul;43(6):1193-206. doi: 10.1085/jgp.43.6.1193.

Abstract

Analyses of ashed muscle tissue show that the uptake of Ca(45) by isolated frog heart ventricles from normal Ringer's solution containing 1 mM Ca reaches a maximum value in about 30 minutes of perfusion which is not exceeded after 3 hours of perfusion. The average amount of this labeled Ca taken up from normal Ringer's is 0.7 mM/kg. wet weight of muscle. In contrast to this, the amount of labeled Ca taken up by ventricles perfused with K-free Ringer's increases at a linear rate over a 60 minute period to twice the normal value coinciding with the gradual development of contracture and coinciding with a cellular K loss and Na gain of about 30 mM/kg. How much of the extra labeled Ca taken up from K-free Ringer's represents a net gain in cellular Ca content is not known. However, evidence has been obtained that some of this labeled Ca enters an intracellular compartment. EDTA in K-free Ringer's solution causes relaxation of ventricles in contracture and also renders the muscle fibers indiscriminately permeable. This indicates that a combination of Ca with sensitive intracellular sites is probably the cause of the K lack contracture.

摘要

对灰化肌肉组织的分析表明,从含有1 mM钙的正常任氏液中分离出的蛙心心室对Ca(45)的摄取在灌注约30分钟时达到最大值,灌注3小时后未超过该值。从正常任氏液中摄取的这种标记钙的平均量为0.7 mM/kg湿肌肉重量。与此相反,用无钾任氏液灌注的心室摄取的标记钙量在60分钟内呈线性增加,达到正常值的两倍,这与挛缩的逐渐发展一致,也与细胞内钾流失和钠增加约30 mM/kg一致。从无钾任氏液中摄取的额外标记钙中有多少代表细胞钙含量的净增加尚不清楚。然而,已经获得证据表明,一些这种标记钙进入了细胞内区室。无钾任氏液中的EDTA会使挛缩的心室内舒张,也会使肌肉纤维无差别地通透。这表明钙与敏感的细胞内位点结合可能是低钾挛缩的原因。

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