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

为了阐明局灶性脑缺血损伤是否能引起周围神经元的缺血耐受，对沙土鼠进行了免疫组织化学和~(31)P-核磁共振波谱研究。采用头颅磁粉-微磁铁颗粒静脉注射或大脑中动脉闭塞的方法诱导右侧皮质脑梗塞。在梗死区和邻近的海马区，未发现HSP70基因的表达。免疫组织化学结果显示，脑梗塞后3d和7d，梗死区及邻近海马区CA1区有GFAP阳性星形胶质细胞聚集。脑梗塞后1、3、7d进行5min前脑缺血可导致非梗死侧CA1区弥漫性神经元死亡。而脑梗塞后3d前脑缺血5min可导致梗死侧CA1区少量神经元死亡。这种缺血耐受性在梗塞附近的CA1区最为显著。脑缺血5min组在脑梗塞后第1天观察到不明显的缺血耐受性。然而，在脑梗塞后7d的缺血5min组，没有观察到这种耐受性。31P-核磁共振研究表明，无论是否存在脑梗塞，前脑缺血均可引起严重的能量紊乱。结果表明，在局灶性脑梗塞后的几天内，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到保护作用。

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.