Fetal Hypoxemia as a Signal for Parturition

Alterations in oxygenation are known to influence directly prostaglandin (PG) production by tissues such as fetal and neonatal lung cells, and by the fetal brain. However, at the present time there is no systematic study of the effects of altered oxygen tensions on PG output by the placenta or fetal membranes, the major sites of eicosanoid generation in the rocesses leading to birth. In comparison, there is considerable evidence that fetal hypoxemia activates components of the fetal hypothalamic-pituitary-adrenal-placental (HPAP) axis, including placental peptide output, and thereby may contribute indirectly to the stimulus to elevated PG generation and myometrial contractility. In this paper we shall consider situations of reduction in oxygenation that may influence HPAP activity. These include alterations in basal partial pressure of oxygen (PaO2) with gestational age, or short-term fluctuations in PaO2 resulting from episodic contractions of the myometrium throughout pregnancy. Second, there may be short-term acute reductions in fetal PaO2, reproduced experimentally in various models of acute fetal hypoxemia. Third, there may be a chronic longer-term impairment of fetal oxygenation, contributing to intrauterine growth retardation and studied experimentally in models of placental embolism, or chronic reductions in uteroplacental blood flow.