ENGINE AND RADIATOR - FETAL AND PLACENTAL INTERACTIONS FOR HEAT DISSIPATION

The 'engine' of fetal metabolism generates heat (3-4 W kg(-1) in fetal sheep) which has to be dissipated to the maternal organism. Fetal hea t may move through the amniotic/allantoic fluids to the uterine wall ( conductive pathway; total conductance, 1.1 W degrees C-1 kg(-1)) and w ith the umbilical arterial blood flow (convective pathway) to the plac enta. Because resistance to heat flow is larger than zero fetal temper ature exceeds maternal temperature by about 0.5 degrees C (0.3-1 degre es C). Probably 85% of fetal heat is lost to the maternal organism thr ough the placenta, which thus serves as the main 'radiator'. Placental heat conductivity appears to be extremely high and this may lead to i mpaired heat exchange (guinea-pig placenta). A computer simulation dem onstrates that fetal temperature is essentially clamped to maternal te mperature, and that fetal thermoregulatory efforts to gain thermal ind ependence would be futile. Indeed, when the late gestational fetus in utero is challenged by cold stress, direct and indirect indicators of (non-shivering) thermogenesis (oxygen consumption, increase of plasma glycerol and free fatty acid levels) change only moderately. In premat urely delivered lambs, however, cold stress provokes summit metabolism and maximum heat production. Only when birth is imitated in utero (by cord clamping, external artificial lung ventilation and cooling) do t hermogenic efforts approach levels typical of extra-uterine life. This suggests the presence of inhibitors of thermogenesis of placental ori gin, e.g. prostaglandins and adenosine. When the synthesis of prostagl andins is blocked by pretreatment with indomethacin, sheep fetuses rea ct to intra-uterine cooling with vigorous thermogenic responses, which can be subdued by infusion of prostaglandin E(2) (PGE(2)). Since the sheep placenta is known to produce sufficient amounts of PGE(2), it se ems that the placenta controls fetal thermogenic responses to some ext ent. This transforms the fetus into an ectothermic organism, and yet a llows the newborn the full exploitation of thermoregulatory responses typical of endothermic animals.