Derewlany L O, Radde I C
Can J Physiol Pharmacol. 1985 Dec;63(12):1577-80. doi: 10.1139/y85-259.
Transplacental 45Ca and 32P flux was measured across the in situ perfused guinea-pig placenta under conditions of acute maternal hypocalcaemia and hypercalcaemia. Maternal hypercalcaemia induced acutely by calcium gluconate infusion caused an increase in maternal-to-fetal 45Ca flux which was proportional to the increase in maternal plasma ionized calcium concentration. Acute maternal hypocalcaemia was induced by EGTA infusion and resulted in a decrease in maternal plasma ionized calcium concentration proportional to a corresponding decrease in transplacental 45Ca transfer. A bolus of calcium gluconate caused a transient decrease in 32P flux, whereas EGTA administration was without significant effect on transplacental 32P transfer. Calcium transport across the placenta is not saturated under conditions of maternal normocalcaemia and may be altered according to acute changes in maternal plasma calcium concentration. Thus, control of maternal-to-fetal calcium transfer does not appear to be at the placental level. This suggests that fetal calcium homeostasis may be regulated by the fetus itself.
在急性母体低钙血症和高钙血症条件下，对原位灌注的豚鼠胎盘进行了经胎盘的45Ca和32P通量测定。通过输注葡萄糖酸钙急性诱导的母体高钙血症导致母体到胎儿的45Ca通量增加，这与母体血浆离子钙浓度的增加成正比。通过输注EGTA诱导急性母体低钙血症，导致母体血浆离子钙浓度降低，与经胎盘45Ca转运的相应降低成比例。推注葡萄糖酸钙导致32P通量短暂降低，而给予EGTA对经胎盘32P转运无显著影响。在母体血钙正常的情况下，钙通过胎盘的转运不饱和，并且可能根据母体血浆钙浓度的急性变化而改变。因此，母体到胎儿的钙转运控制似乎不在胎盘水平。这表明胎儿的钙稳态可能由胎儿自身调节。
