Matsuo Y, Hasegawa K, Doi Y, Kinugasa A, Uchiyama M, Sawada T
Department of Paediatrics, Kyoto Prefectural University of Medicine, Japan.
Eur J Pediatr. 1995 Jul;154(7):571-6. doi: 10.1007/BF02074837.
One of the causes of early onset hyperkalaemia in very low birth weight infants is presumed to be the dysfunction of K+ transport across the cell membrane. Sodium-potassium adenosine triphosphatase(Na(+)-K+ ATPase) is known to play a major role in K+ transport. We compared the concentrations of erythrocyte Na(+)-K+ ATPase (Vmax levels) for hyperkalaemic and normokalaemic infants of matched gestational age. In hyperkalaemic infants, the highest levels of Vmax were reached at 24-48 h after birth, but in normokalaemic infants, there were no significant changes in Vmax levels during the 1st week after birth. At 12-72 h after birth, erythrocyte K+ concentrations for hyperkalaemic infants were higher than those of normokalaemic infants. For both groups of infants, the highest levels of plasma K+ during the 1st week after birth showed a positive correlation with those of Vmax.
Na(+)-K+ ATPase on the cell membrane is activated to compensate for hyperkalaemia; however, when this compensation is incomplete, hyperkalaemia occurs.
极低出生体重儿早期高钾血症的原因之一被认为是钾离子跨细胞膜转运功能障碍。已知钠钾腺苷三磷酸酶（Na(+)-K+ ATPase）在钾离子转运中起主要作用。我们比较了胎龄匹配的高钾血症和正常钾血症婴儿的红细胞钠钾腺苷三磷酸酶浓度（Vmax水平）。在高钾血症婴儿中，出生后24 - 48小时达到最高Vmax水平，但在正常钾血症婴儿中，出生后第一周Vmax水平无显著变化。出生后12 - 72小时，高钾血症婴儿的红细胞钾离子浓度高于正常钾血症婴儿。对于两组婴儿，出生后第一周血浆钾离子的最高水平与Vmax水平呈正相关。
细胞膜上的钠钾腺苷三磷酸酶被激活以代偿高钾血症；然而，当这种代偿不完全时，就会发生高钾血症。
