Source of extracellular brain adenosine during hypoxia in fetal sheep
Source of extracellular brain adenosine during hypoxia in fetal sheep
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DOI：
10.1016/s0006-8993(97)01207-9
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发表时间：
1997-12-19
期刊：
影响因子：
2.9
通讯作者：
Murray, TF
中科院分区：
文献类型：
--
作者：
Koos, BJ;Kruger, L;Murray, TF
进行微透析以确定缺氧是否通过细胞外5'-单磷酸腺苷（5- amp）的去磷酸化增加胎儿脑腺苷（ADO）浓度。当用含有核苷转运蛋白抑制剂的合成脑脊液（CSF）灌注探针时，缺氧（胎儿PaO2，约为14 Torr）使胎儿脑ADO水平增加了两倍，而用这种溶液加外链5′-核苷酸酶（AOPCP）阻滞剂灌注探针则没有增加。缺氧引起的胎儿大脑ADO浓度的升高主要取决于细胞外5'-AMP的水解。(C) 1997爱思唯尔科学有限公司
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.