Roussel S, Pinard E, Seylaz J
Laboratoire de Physiologie et Physiopathologie Cerebrovasculaire, U 182, I.N.S.E.R.M., UA 641 C.N.R.S., Université Paris VII, France.
Brain Res. 1991 Apr 5;545(1-2):171-4. doi: 10.1016/0006-8993(91)91283-7.
The effects of the adenosine agonist, (R)-phenylisopropyladenosine on focal cerebral ischemia induced by middle cerebral artery occlusion were investigated in spontaneously hypertensive rats. The drug was given 30 min before occlusion and each hour thereafter for 6 h. The neurological status of the rats was estimated 2, 24 and 48 h after occlusion. Infarct volumes were measured 48 h after occlusion (Cresyl violet-stained sections). (R)-Phenylisopropyladenosine did not significantly reduce infarct size, nor did it modify the neurological score. As there is considerable evidence of the neuroprotective effects of adenosine in normotensive rats, the present results may be due to a more abrupt reduction in cerebral blood flow in the territory surrounding the ischemic core, where neuroprotection could be expected, in the spontaneously hypertensive rat strain. Consequently, neuroprotection may be more difficult when focal cerebral ischemia is associated with hypertension.
在自发性高血压大鼠中，研究了腺苷激动剂（R）-苯异丙基腺苷对大脑中动脉闭塞所致局灶性脑缺血的影响。在闭塞前30分钟给予该药物，此后每小时给药一次，共给药6小时。在闭塞后2小时、24小时和48小时评估大鼠的神经状态。在闭塞后48小时（用甲酚紫染色切片）测量梗死体积。（R）-苯异丙基腺苷并未显著减小梗死面积，也未改变神经评分。由于有大量证据表明腺苷对正常血压大鼠具有神经保护作用，目前的结果可能是由于在自发性高血压大鼠品系中，缺血核心周围区域的脑血流量更突然地减少，而在该区域有望实现神经保护。因此，当局灶性脑缺血与高血压相关时，神经保护可能更困难。
