ROLE OF PROSTAGLANDIN E(2) AND PROSTACYCLIN IN NONSHIVERING THERMOGENESIS DURING SIMULATED BIRTH IN-UTERO

Prostaglandin E(2) (PGE(2)) inhibits and prostacyclin (PGI(2)), stimul ates lipolysis in vitro. Their role in initiating nonshivering thermog enesis at birth was investigated in 16 fetal sheep at 129-143 days ges tation. In 10 fetuses indomethacin, a prostaglandin synthesis inhibito r, was infused; in 6 fetuses saline was administered as a control. 16 h later birth was simulated in utero. The plasma levels of PGE(2) and PGI(2) were unaffected by cooling. In the control fetuses, ventilation ,vith oxygen caused PGE(2) to fall, PGI(2) to rise, and initiated mode rate thermogenesis, signaled by a twofold increase in plasma free fatt y acids (FFA). After umbilical cord occlusion, PGE(2) decreased furthe r (PGI(2) was unchanged) and thermogenesis accelerated. In indomethaci n-treated fetuses, in which the prostanoids had decreased and remained at similar to 20% normal, cooling initiated moderate nonshivering the rmogenesis, and ventilation and cord occlusion caused no further chang es. Changes in plasma adenosine were similar in control and indomethac in-treated groups. We conclude that declining PGE(2) and rising PGI(2) contribute to the initiation of thermogenesis at birth, but that othe r agents possibly of placental origin may play a contributory role.