Role of vasopressin in mediation of fetal cardiovascular responses to acute hypoxia.

The present study was designed to test the hypothesis that arginine vasopressin mediates the fetal cardiovascular response to acute hypoxia. Chronically catheterized sheep fetuses at 126 to 138 days' gestation were infused with either an arginine vasopressin pressor antagonist (n = 8) or saline solution as control (n = 8). A 30-minute hypoxia was induced by infusion of nitrogen containing 5% carbon dioxide into the maternal trachea. Fetal arterial PO2 decreased 13.1 +/- 1.3 (SE) mm Hg from a basal value of 23.8 +/- 1.5 mm Hg and there was no significant difference in the degree of hypoxia between the two groups. Fetal arterial and venous pressures increased significantly, whereas the blood volume decreased, but these changes were similar between the control and arginine vasopressin-blocked fetuses. Heart rate fell similarly in both groups during hypoxia by an average of 35 beats/min. At the termination of hypoxia, heart rate in the blocked group rebounded to levels significantly above baseline and remained elevated for 30 minutes, whereas heart rate in the control group returned slowly to basal values. Recovery of arterial pressure, venous pressure, and blood volume were similar in the two groups. Thus it appears that arginine vasopressin may mediate in part the fetal heart rate response to acute hypoxia. However, the blood volume, arterial pressure, and venous pressure responses to hypoxia appear to be induced by factors other than arginine vasopressin.