Microdialysis was performed to determine whether hypoxia increases fet
al brain adenosine (ADO) concentration through dephosphorylation of ex
tracellular 5'-adenosine monophosphate (5-AMP). Hypoxia(fetal PaO2, ap
proximate to 14 Torr) increased fetal brain ADO levels similar to 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 hyp
oxia-induced rise in fetal brain ADO concentrations depends critically
upon the hydrolysis of extracellular 5'-AMP. (C) 1997 Elsevier Scienc
e B.V.