论文部分内容阅读
背景:脑缺血后内皮细胞结构和功能的完整性是决定缺血时间窗和出血转化的重要因素。目的:动态观察缺血再灌注内皮细胞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。设计:随机对照实验。单位:暨南大学第二临床学院神经内科。材料:实验于1998-03／1999-03在暨南大学第二临床学院实验动物室完成。选择SD大鼠53只,随机分为9组:①假手术组5只。②缺血3 h 组6只。③缺血3 h再灌3 h组6只。④缺血6 h组6只。⑤缺血6 h再灌3 h组6 R。⑥缺血12 h组6只。⑦缺血12 h再灌3h组6只。⑧缺血24 h组6只。⑨缺血24 h再灌3 h 6只。方法: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,E 5等分切脑,取C片脑组织TIC染色定位边缘区。取D片常规脱水、透明、包埋、切片,苏木精-伊红染色,光镜观察。取B片缺血周围区和中心区脑组织,经固定包埋,半薄切片,超薄切片,透射电镜下观察。主要观察指标:①显微镜下观察不同缺血时间点内皮细胞的变化和出血性梗死发生的时间。②电镜下观察不同缺血时间点内皮细胞的超微结构改变。③电镜下观察紧密连接开放时间。④电镜下观察不同缺血时间点胶质细胞足突层空泡化程度。结果:53只大鼠均进入结果分析。光镜下:缺血3 h即可见神经毡疏松, 小血管周围水肿,缺血12 h再灌3 h可见缺血中心区小动脉破裂出血。电镜下:缺血3 h可见毛细血管内皮细胞核肿胀,胞浆内胞饮增加,足突层空泡化呈+;缺血3 h再灌3 h中心区足突层空泡化呈艹,边缘区呈卅;缺血6 h再灌3 h可见内皮紧密连接开放,足突层空泡化呈卅; 缺血12 h再灌3 h后胞饮明显减少,线粒体肿胀也少见,但紧密连接开放增加,足突层空泡化呈卅-(?)。结论:内皮细胞在缺血3 h即可发生明显的结构变化,缺血6 h可见内皮细胞紧密连接开放,缺血12 h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。
BACKGROUND: The structural and functional integrity of endothelial cells after cerebral ischemia is an important determinant of ischemic time window and hemorrhagic transformation. OBJECTIVE: To dynamically observe the morphological and ultrastructural changes of endothelial cells after ischemia-reperfusion, and to understand the tolerance of endothelial cells to different ischemic time. Design: Randomized controlled experiment. SETTING: Department of Neurology, Second Clinical College, Jinan University. MATERIALS: The experiment was performed in experimental animal room of the Second Clinical College of Jinan University from March 1998 to March 1999. Fifty-three SD rats were randomly divided into 9 groups: ① sham operation group (n = 5). ② ischemia 3 h group 6. ③ ischemia 3 h reperfusion 3 h group 6. ④ ischemia 6 h group 6. ⑤ ischemia 6 h reperfusion 3 h group 6 R. ⑥ ischemia 12 h group 6. ⑦ ischemic 12 h reperfusion 3h group 6. ⑧ ischemia 24 h group 6. ⑨ ischemia 24 h reperfusion 3 h 6 only. Methods: The model of focal cerebral ischemia in rats was established by means of thread plug and cerclage. Coronal plane according to A, B, C, D, E 5 equally divided brain, take C piece of brain tissue TIC staining of the marginal zone. Take D conventional dehydration, transparent, embedded, sliced, hematoxylin-eosin staining, light microscopy. The area surrounding the ischemic area of B and the brain tissue of central area were taken, and fixedly embedded, semi-thin section, ultra-thin section and transmission electron microscope. MAIN OUTCOME MEASURES: ① The changes of endothelial cells and the time of hemorrhagic infarction at different ischemic time points were observed under microscope. ② Electron microscopy under different ischemic time points endothelial cell ultrastructure changes. ③ electron microscopy observation of tight connection open time. ④ Under electron microscope, the degree of vacuolation of glomerulus foot process in different ischemic time points was observed. Results: All 53 rats were involved in the result analysis. Light microscopy: 3 h after ischemia can be seen loose neurofibrils, small blood vessels around the edema, ischemia 12 h reperfusion 3 h visible ischemic arteriolar rupture hemorrhage. Under electron microscope, capillary endothelial cell nucleus was swollen at 3 h after ischemia, while intracytoplasmic pinocytosis was increased. The vacuole of the foot process was +. In the ischemic 3 h, The area was 卅; reperfusion at 6 h after ischemia for 3 h showed endothelial tight junctions open, follicular stump pterygia; ischemia 12 h reperfusion 3 h after drinking significantly reduced mitochondria, mitochondrial swelling is also rare, but closely linked to open Increased, foot process of air bubble was 卅 - (?). CONCLUSION: Endothelial cells undergo obvious structural changes at 3 h of ischemia, endothelial cells are tightly connected and open after 6 h of ischemia, and hemorrhagic transformation occurs after 12 h of ischemia, and the hemorrhagic transformation mostly occurs after reperfusion Central District.