Plasma vasopressin levels during hypoxaemia and the cardiovascular effects of exogenous vasopressin in foetal and adult sheep.

Abstract

Fetal plasma vasopressin levels were measured by bioassay in chronically catheterized sheep from 110-145 days gestation. In fetuses in good condition resting circulating vasopressin concentrations were generally undetectable (< 5 .mu.U[microunits]/ml). In 15% of the samples low concentrations (5-10 .mu.U/ml) were observed. Hypoxemia in the fetus was caused by allowing the ewe to breathe 9% O2-3% CO2 in N2 for 1 h. Plasma vasopressin levels rose in the fetus to 119 .+-. 32 .mu.U/ml, whereas the hormone levels in the ewe were not routinely increased. In the fetus, the rise in plasma vasopressin levels was significantly related to the fall in pH and Pa, O2 [arterial partial pressure of oxygen] during the hypoxia. In fetuses in which the cervical vagosympathetic trunks were cut, the rise in plasma vasopressin levels (to 48 .+-. 25 .mu.U/ml) during hypoxemia was less than in intact fetuses. The increase was related only to the fall in arterial pH and the regression coefficient was less than in intact fetuses. During hypoxemia arterial pressure rose and heart rate fell in the normal fetuses. The rise in arterial pressure was greatest when the plasma vasopressin concentration was highest. Spontaneous episodes of hypoxemia (Pa, O2 < 15 mmHg) and/or acidemia (pH < 7.30) occurred in 4 intact fetuses and 4 fetuses in which the cervical vagosympathetic trunks were cut; all of the latter lambs died in utero. Plasma vasopressin levels were elevated and the concentrations were inversely related to arterial pH. I.v. infusions of vasopressin to fetuses increased plasma vasopressin levels to 6-202 .mu.U/ml; the rate of clearance of the hormone was 3 times that in adult ewes. There was a large increase in arterial pressure and bradycardia. The hypertensive effects of vasopressin were relatively much greater in the fetus than in adult ewes.