Perinatal thermogenesis.

The rapid initiation of thermogenesis is crucial for the survival of newborn infants. At birth the fetus must adapt to cooling, increased oxygenation and separation from the placenta. An experimental approach in the chronically instrumental fetal sheep of 'simulated birth in utero' allowed the evaluation of each of these stimuli sequentially. Cooling stimulated shivering, cardiovascular and endocrine responses but not nonshivering thermogenesis (NST). Ventilation of the cooled fetus with oxygen caused only modest NST which was not altered by an infusion of triiodothyronine. Occluding the umbilical cord was followed by a rapid substantial rise in NST which was maintained until the placental circulation was re-established. Thus the placenta is secreting factors into the fetal circulation which inhibit the ability of the brown adipose tissue to respond to either hormonal or neural stimuli. Placental prostaglandin E2 and probably adenosine are tonic inhibitors of thermogenesis in utero. Effective thermogenesis after birth requires the combination of separation from the placental inhibitors of lipolysis, increased oxygenation from breathing and the stimulation of cutaneous cold receptors.