局灶性脑缺血再灌注内皮细胞缺血耐受性观察

目的 观察脑缺血再灌注内皮细胞的形态学和超微结构变化，了解内皮细胞对不同缺血时间的耐受性。方法 SD大鼠53只，随机分为假手术组、单纯缺血组、缺血再灌注组。采用线栓并环扎的方法建立大鼠局灶脑缺血模型。冠状面按A、B、C、D、E5等分切脑，取C片脑组织TTC染色定位边缘区。取D片常规脱水、透明、包埋、切片，HE染色，光镜观察。B片取缺血周围区和中心区脑组织，经固定包埋，半簿切片1μm，超溥切片JEOL100透射电镜下观察。结果 光镜下：缺血3h可见神经毡疏松，小血管周嗣水肿，缺血12h再灌注3h可见缺血中心区小动脉破裂出血。电镜下：缺血3h可见毛细血管内皮细胞核肿胀，胞浆内胞饮增加，星形胶质足突层空泡化呈＋：缺血3h再灌注3h中心区足突层空泡化呈（＋＋），边缘区呈（＋＋＋）；缺血6h再灌注3h可见内皮紧密连接开放，足突层空泡化呈（＋＋＋）；缺血12h再灌注3h后胞饮明显减少，线粒体肿胀也少见，但紧密连接开放增加，足突层空泡化呈（＋＋＋～＋＋＋＋）。结论 内皮细胞存缺血3h即可发生明显的结构变化，缺血6h可见内皮细胞紧密连接开放，缺血12h后可发生出血性转化，出血转化多发生于再灌注后的缺血中心区。

Tolerance of endothelial cells to ischemia after focal cerebral ischemia-reperfusion

Objective To observe the morphological and ultrastructural changes of endothelial cells and to explore the tolerance of endothelial cells to ischemia at different time points after cerebral ischemia-reperfusion. Methods 53 SD rats were randomly divided into 3 groups: sham-operation, ischemia and ischemia-reperfusion. The model of local cerebral infarction was established by the thread-embolization and cerclage. Their brains were sliced evenly into A, B, C, D and E segment along the coronal plate. Segment C of the cerebral tissue was TTC stained for localizing the ischemia margin. Segment D was dehydrated routinely, embeded, sliced, followed by HE staining and observation under light microscope. Segment B was treated by obtaining the tissues around ischemia and the central cerebral tissues, fixing and embediing them for ultrathin section and then observing the sections under JEOL100 transmission electron microscope. Results Observation under light microscope showed Neuropil rarefaction and edema around small vessels were observed 3 h after ischemia. Rupture and hemorrhage of the small arteries in core regions 3 h after ischemia and 3 h reperfusion. Observation under electron microscope showed nucleus swelling, enhanced pinocytosis, foot process vacuoles of astrocyte (+) 3 h after ischemia; foot process vacuoles of astrocyte was (++) in center to (+++) in margins 3h after ischemia and 3 h reperfusion; endothelial tight junction opened and foot process vacuoles of astrocyte was (+++) 6 h after ischemia and 3 h reperfusion. Besides, pinocytosis and swelling of mitochondrion decreased, but tight junction opening increased 12 h after ischemia and 3 h reperfusion, with foot process vacuoles of astrocyte (+++ to ++++). Conclusion 3 h after ischemia, the changes of endothelial cells are evident in structure. Tight junction of endothelial cells is broken 6 h after ischemia. Hemorrhage can be seen 12 h after ischemia and it often occurs in the central regions after ischemia-reperfusion.