Effects upon the fetus of oxygen administration to the mother. A study in monkey.
Catheters were placed into assorted arteries and veins of 8 anaesthetized pregnant monkeys and their fetuses. Oxygen-sensitive electrodes were also inserted subcutaneously into 3 of the 8 fetuses. Periodic samples of maternal and fetal blood were analyzed for PO2, PCO2 and pH. Oxygen administration to the mothers reliably increased the PO2 of blood taken from the fetal carotid artery and less constantly augmented the PO2 of blood withdrawn from the femoral artery and vein. During 5-6 hours of study the oxygen tension of fetal blood samples of all animals progressively declined. However, the most marked declines in PO2 values at all fetal sites were regularly observed at those times as--or after--the mothers emerged from anaesthesia. At these times also the magnitudes of the increases in fetal blood PO2 brought about by administering oxygen to the mothers diminished markedly and in parallel at all sample sites. The closely similar magnitudes of these various reductions at all fetal sample sties indicate that the basic mechanisms leading to decreased oxygen delivery lie outside the fetuses and are most likely due to decreased maternal blood flow to the uterus because of increased maternal sympathetic stimulation. These reductions in oxygen delivery to the fetus are all regularly reversed by reanasthetizing the mothers. The studies carried out with oxygen-sensitive electrodes demonstrate that administering oxygen to the mothers regularly increases oxygen tension of fetal tissues but after a 50 sec delay.
Effects upon the fetus of oxygen administration to the mother. A study in monkey. Catheters were placed into assorted arteries and veins of 8 anaesthetized pregnant monkeys and their fetuses. Oxygen-sensitive electrodes were also inserted subcutaneously into 3 of the 8 fetuses. Periodic samples of maternal and fetal blood were analyzed for PO2, PCO2 and pH. Oxygen administration to the mothers reliably increased the PO2 of blood taken from the fetal carotid artery and less constantly augmented the PO2 of blood withdrawn from the femoral artery and vein. During 5-6 hours of study the oxygen tension of fetal blood samples of all animals progressively declined. However, the most marked declines in PO2 values at all fetal sites were regularly observed at those times as--or after--the mothers emerged from anaesthesia. At these times also the magnitudes of the increases in fetal blood PO2 brought about by administering oxygen to the mothers diminished markedly and in parallel at all sample sites. The closely similar magnitudes of these various reductions at all fetal sample sties indicate that the basic mechanisms leading to decreased oxygen delivery lie outside the fetuses and are most likely due to decreased maternal blood flow to the uterus because of increased maternal sympathetic stimulation. These reductions in oxygen delivery to the fetus are all regularly reversed by reanasthetizing the mothers. The studies carried out with oxygen-sensitive electrodes demonstrate that administering oxygen to the mothers regularly increases oxygen tension of fetal tissues but after a 50 sec delay.