HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Baillie, P. Articles by Richards, R. Search for Related Content PubMed PubMed Citation Articles by Baillie, P. Articles by Richards, R.

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 CO₂ 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} 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.