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 |
|---|---|
| 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 |
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All Science Journal Classification (ASJC) codes
- Neuroscience(all)
Cite this
Source of extracellular brain adenosine during hypoxia in fetal sheep. / Koos, Brian J.; Kruger, Lawrence; Murray, Thomas F.
In: Brain Research, Vol. 778, No. 2, 19.12.1997, p. 439-442.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Source of extracellular brain adenosine during hypoxia in fetal sheep
AU - Koos, Brian J.
AU - Kruger, Lawrence
AU - Murray, Thomas F.
PY - 1997/12/19
Y1 - 1997/12/19
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0031578865&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0031578865&partnerID=8YFLogxK
U2 - 10.1016/S0006-8993(97)01207-9
DO - 10.1016/S0006-8993(97)01207-9
M3 - Article
C2 - 9459565
AN - SCOPUS:0031578865
VL - 778
SP - 439
EP - 442
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 2
ER -