论文部分内容阅读
经历了慢性缺血后的脑组织在灌注恢复正常时有可能发生严重的脑水肿甚至脑出血,临床上将这种现象称为“正常灌注压突破”(normal perfusion pressure breakthrough,NPPB。通过在实验动物颈部建立颈总动脉-颈外静脉瘘并饲养14周后快速阻断其瘘口,模拟了临床上引起 NPPB 的条件和过程。通过对实验动物脑组织进行电镜检查,发现慢性缺血可引起脑组织内毛细血管内皮细胞变性等结构缺陷,以及毛细血管周围的水肿样改变,内皮细胞的紧密连接疏松,部份标本中红细胞“逸出”管外被周细胞吞噬,可能是 NPPB 超微结构方面的证据。
After experiencing chronic ischemic brain tissue may have severe cerebral edema or even cerebral hemorrhage when perfusion is normal, and this phenomenon is clinically referred to as “normal perfusion pressure breakthrough” (NPPB.) The establishment of carotid arteries-external jugular fistula in the neck of experimental animals and fasting of the fistula after 14 weeks of feeding simulated the clinical conditions and process of causing NPPB.Experimental animal brain tissue by electron microscopy and found that chronic lack Blood can cause structural defects such as degeneration of capillary endothelial cells in the brain tissue, as well as edema-like changes around the capillaries, tight junctions between endothelial cells loose, some of the specimens in the red blood cells “escape ” outside the pericytes may be phagocytosed, may Is evidence of NPPB ultrastructure.