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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 439-442 |
| Number of pages | 4 |
| Journal | Brain Research |
| Volume | 778 |
| Issue number | 2 |
| DOIs | |
| State | Published - Dec 19 1997 |
| Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology
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Cite this
Koos, B. J., Kruger, L., & Murray, T. F. (1997). Source of extracellular brain adenosine during hypoxia in fetal sheep. Brain Research, 778(2), 439-442. https://doi.org/10.1016/S0006-8993(97)01207-9