Maternal hyperventilation and foetal hypocapnia in sheep.

1. In anaesthetized foetal lambs near term, hypocapnia induced by maternal hyperventilation abolished the rise of arterial pressure and femoral vasoconstriction caused by hypoxaemia. This is consistent with interaction of P(CO2) and P(O2) on the foetal aortic bodies.2. In immature lambs (0.6-0.77 of term) maternal hyperventilation caused a fall in foetal carotid P(CO2) commensurate with that in the maternal blood. In mature lambs (at 0.9 or more of term) the fall in foetal carotid P(CO2) was less than that in maternal blood, whether the foetus was exteriorized or in utero.3. The mean transplacental gradient for P(CO2) (maternal arterial-umbilical vascular), when the foetus was replaced with a mechanical pump recirculating foetal blood, was 6.3 mm Hg. This is attributed to placental CO(2) production, and is nearly half the mean P(CO2) gradient (maternal artery-foetal carotid) of about 14 mm Hg during normal maternal ventilation.4. The mean maternal-umbilical transcotyledonary venous gradients (avoiding vascular shunts through the myometrium and intercotyledonary chorion) were for P(CO2) 1.7 mm Hg and for P(O2) 13.4 mm Hg.5. Maternal hyperventilation (P(a, CO2) approximately 20 mm Hg) caused a small fall in mean foetal carotid P(O2) (5 mm Hg), which was readily reversible with no evidence of progressive acidaemia.