STUDY OF CEREBRAL ISCHEMIC TOLERANCE USING MAGNETIC RESONANCE AND IMMUNOHISTOCHEMICAL TECHNIQUES : PART 1

为了阐明局灶性缺血损伤是否会引起周围神经元的缺血耐受，我们对蒙古沙鼠进行了免疫组织化学和31p-NMR光谱研究。颅骨磁分磁铁矿颗粒静脉注射法或大脑中动脉闭塞法诱发右侧皮质梗死。梗塞未引起梗死区及邻近海马区HSP70 mRNA的表达。免疫组织化学研究显示，梗死后3天和7天，梗死区和邻近海马CA1区有gmap阳性星形胶质细胞聚集。在梗死后1、3或7天进行的5分钟前脑缺血可导致非梗死侧CA1区弥漫性神经元死亡。然而，梗死后3天5min前脑缺血导致梗死侧CA1区少量神经元死亡。这种缺血耐受性在梗死附近的CA1区最为显著。梗死后1天缺血5分钟组缺血耐受性较弱。然而，在梗死后7天缺血5分钟组中，没有观察到这种耐受性。核磁共振（31P-NMR）研究表明，无论梗死是否存在，前脑缺血都会引起严重的能量障碍。结果表明，在局灶性梗死后的数天内，周围区域的神经元可能表现出缺血耐受。这种耐受性不是由于热休克蛋白的诱导或能量衰竭的改善。推测，反应性萎缩细胞可能对邻近神经元起保护作用。

In order to clarify wehther focal ischemic insults can cause ischemic tolerance in neurons in the surrounding areas, immunohistochemical and 31p-NMR spectroscopic studes were undertaken in mongolian gerbils. Right cortical infarction was induced by skull magnet-minute magnetite particle intravenous injection methods or middle cerebral artery occlusion. The infarction was found to cause no induction of HSP70 mRNA in infarcted areas and the adjacent hippocampus. Immunohistochemical studies showed GFAP-positive astrocytes accumulation in the infarcted area and the adjacent hippocampal CA1 sectros at 3 and 7 days after infarction. 5-min forebrain ischemia conducted at 1,3 or 7 days after infarction caused diffuse neuronal death in the non-infarcted side CA1 sectors. However, 5 min forebrain ischemia at 3 days after infarction brought about small number of neuronal death in the infarcted side CA1 sector. This ischemic tolerance was most remarkable in the CA1 sector adjacent the infarction. Less prominent ischemic tolerance was observed in a group with 5-min ischemia at 1 day after infarction. Yet, no such tolerance was observed in agroup with 5 min ischemia at 7 days after infarction. 31P-NMR studies indicated that forebrain ischemia caused severe energy disturbance irrespectively of existence of infarction. The results suggest that during several days after focal infarction, neurons in the surrounding areas may show ischemic tolerance. This tolerance is not attributable to induction of heat-shock protein or improvement of energy failure. Presumably, reactive atrocytes may exert protective effects on the adjacent neurons.