Objective:
The purpose of this study was to determine fetal endocrinological and biophysical responses to the further reduction in oxygenation following prolonged nonacidemic hypoxemia in fetal goats. Methods: Seven further hypoxic experiments were performed after prolonged (24-h) nonacidemic hypoxemia, caused by an infusion of nitrogen into the maternal trachea and by reducing uterine arterial blood flow in four chronically instrumented goat fetuses at 123-131 days' gestation. We measured arginine vasopressin, adrenocorticotropic hormone, cortisol, and cathecolamines as endocrinological parameters. Fetal heart rate, fetal blood pressure, and fetal breathing movement were observed as biophysical parameters. Results: Fetal arterial pO 2 was significantly decreased from 27.0 Ϯ 1.2 mmHg (control) to 18.0 Ϯ 0.7 mmHg and 11.3 Ϯ 1.3 mmHg at the end of the prolonged hypoxemia and the further hypoxia, respectively. The further hypoxia induced reductions in fetal heart rate, increases in fetal blood pressure, and a series of gasping. Arginine vasopressin and cathecolamines were elevated significantly by the further hypoxia. Although adrenocorticotropic hormone and cortisol were increasingly elevated, they did not reach a significant level. Conclusions: Some specific fetal responses-excessive elevations of fetal cathecolamines, arginine vasopressin, accompanied with fetal gasping-were observed during further severe hypoxia.