大鼠局灶性脑缺血-再灌注损伤组织病理及超微结构研究

为探讨脑缺血—再灌注损伤病理机制进行实验性研究。方法　应用鼠大脑中动脉局灶脑缺血—再灌注模型 ,进行组织病理超微结构研究。结果　①缺血 1、2小时再灌注脑损伤最轻 ,缺血 4小时再灌注脑损伤最重 ,中性粒细胞出现在缺血损伤区 ,与单纯缺血 4小时损伤程度相当。②缺血 1小时再灌注 ,凋亡细胞最多 ;缺血 2小时再灌注 ,凋亡细胞少于缺血 1小时再灌注组 ;缺血 3小时再灌注 ,凋亡细胞几乎是缺血 1小时再灌注组的 1/ 4,并与坏死细胞掺杂 ;缺血 4小时再灌注 ,凋亡细胞不存在 ,主要以坏死细胞为主。结论　缺血性损伤发生不可逆时 ,在损伤中心区有中性粒细胞出现 ,循环破坏严重。不同强度的缺血导致细胞凋亡的发生从缺血损伤中心到半暗带 ,较温和的脑缺血损伤以细胞凋亡为主 ,剧烈脑缺血损伤以细胞坏死为主 ,坏死细胞的出现与中性粒细胞的出现相伴随

Rat focal cerebral ischmia-reperfusion injury pathological maolecular injury and ultrastructure of histopathology experimental study

Objective To probe into focal cerebral ischmia-reperfusion injury pathological maolecular injury in experimental study.Method It was applaied that pathological model of cerebral ischmia reperfusion to objective ultrastructure of histopathology.Results One hour and two hours ischmia following reperfusion cerebral injury were lightest,4 h ischmia following reperfusion cerebral injury was heavist,neutrophilic granulocyte emerged in ischemial injury region,corresponded to purely 4 h cerebral ischmia.One hour ischmia following reperfusion apoptosis was at the peak,2 h ischmia following reperfusion apoptosis was fewer 1 h than 1 h ischmia following reperfusion gooupe,3 h ischmia following reperfusion gooupe apoptosis was in the 1 h ischmia following reperfusion gooupe of one to four,and mixed up necrosis cell,4 h ischmia following reperfusion cerebral injury took necrosis cell as the dominant and no apoptosis.Conclusions Ischemic injury was no reverse that there were neutrophilic granulocyte emerged in,and injuried circulation,and apoptosis was majio in mild ischemic,necrosis cell and neutrophilic granulocyte emerged in ischemial injury region.