Maternal psychological stress and fetal asphyxia: a study in the monkey.

Fifteen pregnant rhesus monkeys near term were anesthetized with pentobarbital. Catheters were placed into the right femoral arteries of the mother and fetus, the fetuses being retained in utero. After repair of all incisions, the mothers were placed on their sides and allowed to recover from anesthesia. As they awakened, their fetuses regularly developed blood chemical and, frequently, vital signs changes indicative of deepening asphyxia. In eight cases, anesthesia was reinstated with intravenous pentobarbital, 30 mg. per kilogram. This caused an immediate and significant improvement in oxygenation of the fetus in all instances. The remaining animals were transferred to restraining chairs where the blood chemical and cardiovascular statuses of the mothers and fetuses were followed over the next 3 to 72 hours. During this time, the mothers, fully awake, were subjected to both "contrived" and "incidental" episodes of psychological stress stimulation. In the majority of instances, these periods of stress to the mothers caused episodes of bradycardia and hypotension in their fetuses. These induced vital signs changes of the fetuses appeared regularly about 50 seconds after the beginning of the periods of stress stimulation of the mother. Similarly, the vital signs changes frequently began returning toward more normal values with 1 to 2 minutes after the alleviation of maternal stress. Blood samples drawn in single cases before, during, and after recovery from bradycardia identified an associated increase in asphyxia of the fetuses. These episodic aggravations of the already existent fetal asphyxia of the fetuses. These episodic aggravations of the already existent fetal asphyxia brought about by stress stimulation of the mother are interpreted as resulting from activation of the maternal sympathetic nervous system causing vasoconstriction throughout the abdominal viscera and an accompanying retardation in intervillous space perfusion.