Release of Vasopressin by the Fetal Lamb during Premature Parturition Induced with Corticotropin

Abstract
Summary: These studies were implemented to assess the relationship between fetal vasopressin secretion and the progression of parturition as well as the contribution of specific stimuli to vasopressin release during labor. In chronically catheterized fetal lamb preparations, labor was induced by infusion of adrenocorticotropin (12.5 mg/kg/hr) to seven fetuses at 130 ± 1 day of gestation. Before labor, fetal plasma vasopressin concentrations were 2.1 ± 1.4 pg/ml and remained low (5.3 ± 3.4 pg/ml) during prodromal and early phases of labor, but rose significantly in the active and expulsive phases (39.6 ± 27.5 and 173.3 ± 152.9 pg/ml) to reach peak values at delivery (584.2 ± 433 pg/ml) and decrease by 30 min after birth (359.8 ± 90.0 pg/ml). At delivery, fetal plasma vasopressin concentrations were strongly correlated (P < 0.001) with hormone values obtained during the latter phases of labor. Fetal arterial pH and oxygen tension was inversely correlated with plasma vasopressin (P < 0.01). No similar correlations were found with arterial P CO 2 , K, Na, Cl, osmolality, or packed cell volume. Unexpectedly, we observed a significant (P < 0.001) and progressive decrease in fetal oxygen tension during the induction process. Other characteristics of adrenocorticotropin-induced parturition seemed to mimic those of spontaneous labor. Speculation: Many of the biophysical and biochemical changes that occur during spontaneous term labor in the sheep can be studied in a more controlled fashion during premature labor induced by infusion of adrenocorticotropin to the fetus. Vasopressin hypersecretion during the latter stages of labor is in part mediated by hypoxia. The elevated plasma hormone concentrations may play a major role in the fetal cardiovascular response to hypoxia including the redistribution of cardiac output. The progressive gradual decrease in fetal oxygen tension noted before the onset of labor may be related to morphologic changes at the fetal maternal interface in the placenta.