Paradoxical rise in brainstem PO(2) following umbilical cord occlusion in full-term rat fetuses

Although the fetus experiences severe hypoxia and ischemia during delivery, the fetal brain is protected from hypoxic-ischemic insults by unknown mechanisms. To investigate this phenomenon, fetal asphyxia was induced in pregnant rats by occlusion of the umbilical cord. Rather than producing cerebral hypoxia, the brainstem PO(2) of at-term fetuses increased following umbilical cord occlusion, while brainstem blood flow was markedly reduced. This paradoxical increase in brainstem PO(2) during asphyxia occurred in the majority of at-term fetuses, less frequently in fetuses 1 day prior to term and did not occur in animals following birth. Because occlusion of the umbilical cord prevents maternal delivery of oxygen to the fetus, we propose that the ability to maintain PO(2) is the result of pre-existing fetal stores of oxygen or from de novo generation of oxygen in the fetal brainstem.