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采用线栓法制备大鼠大脑中动脉栓塞(middlecerebralarteryocclusion,MCAO)模型,在额叶皮层用KCl诱导产生皮层扩散性抑制(corticalspreadingdepression,CSD)。MCAO4h后,利用550nm内源信号光学成像(opticalintrin-sicsignalimaging,OISI)监测局灶性脑缺血后大鼠顶-枕叶皮层内源光信号变化。成像1h内观测到一系列诱导CSD波(14±3次),CSD波局限于顶-枕叶皮层中央区域扩展,以光强的显著下降为特征;而旁侧区域光强无明显改变,不具备CSD波特征,表明CSD波未传播到该区域。随后TTC染色证明上述旁侧区域已经梗死。实验表明:MCAO后4h,皮层区域旁侧部分会梗死;CSD波的OIS变化可用来区分缺血梗死区和外周供血较为完整区域(未梗死区)。
The rat model of middle cerebral artery occlusion (MCAO) was established by thread occlusion. Corticalspreading depression (CSD) was induced by KCl in the frontal cortex. After MCAO4h, the changes of endogenous optical signal in the apex - occipital cortex of rats after focal cerebral ischemia were detected by 550nm internal optical imaging (opticalintrin-sicsignalimaging, OISI). A series of induced CSD waves (14 ± 3) were observed within 1 h of imaging. The CSD wave was limited to the central region of the top-occipital cortex, which was characterized by a significant decrease of light intensity. The light intensity of the lateral region did not change significantly. The CSD wave features indicate that the CSD wave did not propagate to this region. Subsequent TTC staining demonstrated that the above-mentioned lateral region had been infarcted. Experiments show that: 4h after MCAO, part of the cortical area infarction will be infarction; CSD wave OIS changes can be used to distinguish between ischemic infarction and peripheral blood supply is more complete (non-infarcted area).