SUMMARY1. The purpose of this investigation was to determine the effects of maternal hyperoxaemia and hypercapnia on the uterine vascular bed and foetal oxygenation in the large white sow at 80-90 days gestation.2. When maternal hyperoxaemia was induced with 100 % oxygen, there was a highly significant rise in the maternal arterial oxygen tension, but no other significant blood gas or vascular changes were observed.3. When mild maternal hypercapnia was superimposed on maternal hyperoxaemia (oxygen plus 6 % carbon dioxide), the oxygen tension and saturation of both the maternal uterine venous and foetal umbilical venous bloods were significantly increased. Similar but more pronounced increases were found when severe hypercapnia was induced (oxygen plus 50 % carbon dioxide) but in this case all blood samples showed dramatic changes in Pco, and pH. These changes were accompanied by an increase in the systemic blood pressure and uterine blood flow, and a decrease in uterine vascular resistance. 4. When mild hypercapnia was induced without hyperoxaemia (air plus 5 % carbon dioxide) significant increases were recorded in the oxygen tension and saturation of uterine venous and foetal umbilical venous bloods. Systemic and uterine arterial blood pressure rose, the uterine blood flow increased, and uterine vascular resistance fell. 5. It was concluded that the increased foetal oxygen tension during maternal hypercapnia was the result of the increased uterine blood flow and greater mass delivery of oxygen to the placenta, so that once the oxygen requirements of the placental tissues themselves were exceeded there would be an increased oxygen gradient at the site of gas exchange.

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A fixed volume gas exchanger has been constructed from sintered nickel plates and compared with the reservoir gas exchanger previously described. Satisfactory gas exchange was obtained through the plates, but it is difficult to define the characteristics of the apparatus quantitatively.Raising the arterial resistance reduced the 'umbilical' blood flow through both exchangers. With the reservoir exchanger, raising the 'amniotic' pressure reduced the flow of blood through the foetus. 'Umbilical' venous pressure increased and 'umbilical' arterial pulse pressure fell and foetal volume decreased. Lowering the 'amniotic' pressure decreased the 'umbilical' arterial flow but increased 'umbilical' venous flow, so that foetal volume increased. 'Umbilical' venous pressure decreased and 'umbilical' arterial pulse pressure increased.With the fixed volume exchanger, raising the 'amniotic' pressure reduced the flow of blood through the external circuit. 'Umbilical' arterial and venous mean pressures increased and arterial pulse pressure slightly increased. Decreasing the 'amniotic' pressure increased the flow of blood through the external circuit 'Umbilical arterial and venous mean pressures were reduced and there was a small increase of arterial pulse pressure.IN a 'Progress Report' on the work with artificial placentae [Lawn and McCance, 1964] it was stated that a new form of gas exchanger was being developed. This was referred to as placenta B and it was pointed out that the preliminary results showed that the mechanics of the foetal circulation and even the mode of death were affected by the exchanger used. It was clear that there might be much to learn about the fretal circulation from a study of these differences, and the present report contains a description of the new exchanger, placenta B, and a comparision of some of the results obtained by it with those obtained by placenta A (Lawn and McCance, 1962].In the original apparatus the foetal heart pumped the blood into a cylindrical chamber, mounted horizontally, in which multiple discs, partially immersed in a shallow reservoir of blood, rotated slowly in the gas mixture being used for the exchange. The gas was in direct contact with the blood which was returned from the reservoir to the foetus by gravity. This allowed the volume of blood in the fcetus to vary with the tone of the vessels and the venous pressure which had to be set at the discretion of the operator. The correct height was always a problem and placenta B was designed partly in the hope of getting a more physiological external circuit. It consists of a closed external circulation with a sufficiently low resistance to the blood flow to enable the fletal heart to maintain the circulation, at any rate for some hours. The gas exchange takes place through the pores of rigid sintered nickel plates which necessarily maintain the volume of blood in the placenta almost 157 I 0-8