Abstract
Microdialysis was performed to determine whether hypoxia increases fetal brain adenosine (ADO) concentration through dephosphorylation of extracellular 5'-adenosine monophosphate (5-AMP). Hypoxia (fetal PaO2 ≃ 14 Torr) increased fetal brain ADO levels ~ two-fold when the probes were perfused with synthetic cerebrospinal fluid (CSF) containing inhibitors of the nucleoside transporter but not with this solution plus a blocker of ecto- 5'-nucleotidase (AOPCP). The hypoxia-induced rise in fetal brain ADO concentrations depends critically upon the hydrolysis of extracellular 5'- AMP.