REDUCED TRANSFER OF CALCIUM ACROSS THE IN SITU PERFUSED PLACENTAE OF INTRAUTERINE GROWTH RETARDED (IUGR) RAT FETUSES

Abstract

Neonatal rickets has been associated with IUGR secondary to conditions of reduced utero-placental blood flow during pregnancy, e.g., toxemia. There are no studies of calcium transport in IUGR. To test the hypothesis that chronic reduction in utero-placental blood flow impairs materno-fetal calcium transfer, placental calcium transfer was studied using an in situ placental perfusion technique (Mughal et al, 1986, J Physiol 377, 5 P) in rats where IUGR was induced by bilateral uterine artery ligation on day 17 of gestation, & in control animals. On day 20 of gestation (term=22 days), animals were anesthetised with intraperitoneal sodium thiobutabarbitol & fetal circulation of one of the placentas (PI) was perfused via an umbilical artery cannula with Kreb's Ringer solution. 45Ca & 51Cr-EDTA (diffusional marker) were injected into the mother, & their steady state clearance (C1) from maternal circulation to perfusate was calculated from samples collected from a cannula in the umbilical vein. (mean ± SEM) Thus, the total fetal calcium is reduced in IUGR fetuses; the reduction was proportionate to body weight reduction. The steady state materno-perfusate transfer of calcium, but not the diffusional marker, is markedly reduced across placenta of growth retarded fetuses, presumably due to diminished active placental transfer of calcium.