Maternal endocrine and fetal metabolic responses to heat stress.

Heat-stressed pregnant ewes deliver intrauterine growth-retarded lambs. Selected maternal and fetal changes were investigated during acute heat stress in order to elucidate the mechanism for this growth retardation. Uterine blood flow decreased 20 to 30% in pregnant ewes during 1 degree C increases in core temperature. The decreases were accompanied by 60 and 100% increases in serum oxytocin and antidiuretic hormone, respectively. These effects were mimicked by salt loading or injections of antidiuretic hormone or oxytocin, suggesting a role for either or both hormones in regulating uterine blood flow during pregnancy. Chronically heat-stressed pregnant ewes were delivered by Caesarean section. Their fetuses were approximately 20% smaller than thermoneutral controls. Within each pair of heat-stressed twins, one fetus weighted one-third less than its litter mate. No difference in weights were observed within the control twins. The livers and brains of the heat-stressed fetuses were disproportionate in size. The livers from the small heat-stressed twins contained only one-half the protein of the controls and one-fourth the protein of their litter mates. Muscle protein was decreased in the heat-stressed fetuses, and liver and muscle glycogen were elevated as were liver arginase, glutamate-pyruvate transaminase and muscle creatinine. These results are consistent with the following hypothesis: heat stress stimulates the release of maternal antidiuretic hormone or oxytocin, which reduces uterine blood flow and causes a shift in fetal metabolism from anabolic to catabolic pathways; one fetus of heat-stressed twins is more severely affected than its litter mate.