The effects of hypoxaemia in fetal sheep.

Abstract

Fetal hypoxaemia may result from altered maternal PaO2 or a reduction in maternal placental or umbilical blood flow. It is also possible that reduction of gas exchange across the placenta could limit the oxygen supply to the fetus. In this review we will be concerned with the effects of hypoxaemia in fetal sheep during the latter half of pregnancy. At present it is not easy to reduce maternal placental blood flow experimentally in a controlled manner, while an acute restriction of umbilical blood flow results in asphyxia (Towell and Salvador, 1974). Fetal hypoxaemia can be induced reproducibly by lowering maternal inspired oxygen concentrations and hence PaO2. During such experiments, the fetal blood gas tensions take several minutes to equilibrate while the cardiovascular and plasma changes require up to 60 min to reach a relatively steady state (Boddy et al, 1974a; Cohn et al, 1974; Jones and Robinson, 1975; Rurak, 1976a and b; Jones, 1977). Although the acute episodes of hypoxaemia known to occur spontaneously last only a few minutes (Jones and Ritchie, 1976; Patrick et al, 1976), studying changes over a 60-min period provides more detailed information. A different approach has been used to produce long-term hypoxaemia in the fetus so as to minimize the effects on the mother. This has been either to reduce placental mass surgically (Alexander, 1964), to embolize the maternal placenta with microspheres (Creasy et al, 1972), or to reduce umbilical blood flow by umbilical artery ligation (Emmanouilides et al, 1968). It is important when investigating fetal hypoxaemia to avoid the effects of anaesthesia and surgery. Such acute experiments are associated with much higher hormone (at least 10 fold higher for ACTH, catecholamines and vasopressin) and metabolite concentrations than in chronically catheterized fetal preparations. For instance, the plasma catecholamine concentration in the exteriorized fetal sheep is higher than that normally seen during hypoxaemia in fetal sheep in utero (Jones and Robinson, 1975; Jones and Rurak, 1976a) and hypoxaemia causes a tachycardia in the exteriorized fetus compared with an initial bradycardia in utero. We will therefore concentrate on the cardiovascular, metabolic and endocrine changes observed with both short-term and chronic hypoxaemia in the conscious unrestrained sheep with implanted catheters.