Source of extracellular brain adenosine during hypoxia in fetal sheep
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作者:
Koos, BJ
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Univ Calif Los Angeles, Dept Obstet & Gynecol, Nicholas S Assali Perinatal Res Lab, Sch Med, Los Angeles, CA 90095 USAUniv Calif Los Angeles, Dept Obstet & Gynecol, Nicholas S Assali Perinatal Res Lab, Sch Med, Los Angeles, CA 90095 USA
Koos, BJ
[1
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Kruger, L
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机构:Univ Calif Los Angeles, Dept Obstet & Gynecol, Nicholas S Assali Perinatal Res Lab, Sch Med, Los Angeles, CA 90095 USA
Kruger, L
Murray, TF
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机构:Univ Calif Los Angeles, Dept Obstet & Gynecol, Nicholas S Assali Perinatal Res Lab, Sch Med, Los Angeles, CA 90095 USA
Murray, TF
机构:
[1] Univ Calif Los Angeles, Dept Obstet & Gynecol, Nicholas S Assali Perinatal Res Lab, Sch Med, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Dept Neurobiol, Inst Brain Res, Sch Med, Los Angeles, CA 90095 USA
[3] Oregon State Univ, Coll Pharm, Corvallis, OR 97331 USA
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, approximate 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 hypoxia-induced rise in fetal brain ADO concentrations depends critically upon the hydrolysis of extracellular 5'-AMP. (C) 1997 Elsevier Science B.V.