Roucher P, Méric P, Corrèze J L, Mispelter J, Tiffon B, Lhoste J M, Seylaz J
Laboratoire de Physiologie et Physiopathologie Cérébrovasculaire, INSERM U182-CNRS UA641, Paris, France.
J Cereb Blood Flow Metab. 1991 May;11(3):453-8. doi: 10.1038/jcbfm.1991.87.
The metabolic effects of R-phenylisopropyladenosine (R-PIA), an agonist of adenosine A1 receptors, were studied by in vivo 31P NMR spectroscopy before, during, and after 30 min of reversible forebrain ischemia in the rat. R-PIA had no effect on cerebral metabolism before ischemia. During a 30-min ischemia, R-PIA reduced the decrease in phosphocreatine (43 +/- 11% of the control level at the end of ischemia vs. 27 +/- 9% in the reference group) and ATP (58 +/- 12% vs. 40 +/- 23%) and the increase in inorganic phosphate (672 +/- 210% vs. 905 +/- 229%). The intracellular acidosis elicited by ischemia was also less in the treated group (pH of 6.40 +/- 0.10 vs. 6.30 +/- 0.10). Recirculation was associated with a faster recovery of PCr, ATP, Pi, and pHi to control levels in the treated group than in the reference group. It is concluded that adenosine protects against ischemic injury by mechanisms that include metabolic protection.
采用体内31P核磁共振波谱法,研究了大鼠可逆性前脑缺血30分钟前、期间及之后,腺苷A1受体激动剂R-苯异丙基腺苷(R-PIA)的代谢效应。缺血前,R-PIA对脑代谢无影响。在30分钟的缺血期间,R-PIA减少了磷酸肌酸(缺血结束时为对照水平的43±11%,而参照组为27±9%)和三磷酸腺苷(ATP)(58±12%对40±23%)的降低,以及无机磷酸盐的增加(672±210%对905±229%)。治疗组中,缺血引发的细胞内酸中毒也较轻(pH值为6.40±0.10,而参照组为6.30±0.10)。再灌注时,与参照组相比,治疗组的磷酸肌酸、ATP、无机磷酸盐和细胞内pH值恢复至对照水平的速度更快。得出结论:腺苷通过包括代谢保护在内的机制预防缺血性损伤。