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脑水肿为决定急性脑血管病情的重要因素之一。依病理分血管源性和细胞毒性。前者由于血脑屏障破坏,毛细血管紧密接点分离,血浆成分向周围细胞外间质漏出引起。后者为血管内皮细胞、神经胶质细胞、神经细胞肿胀,其机制为缺血,脑能量代谢降低,Na泵障碍、水钠流入细胞所致。缺血性脑水肿始以细胞毒性,继之血管源性。但是最近提出可能跟自由基反应所致的细胞膜障碍有关。因缺血而产生的自由基跟构成活体膜的多价不饱和脂肪酸反应制造过氧化酯,引起细胞膜障碍,以线粒体、溶酶体为主构成的血脑屏障膜也损害。另外还有人认为自由基反应是因缺血向障碍脑组织再供
Brain edema is one of the important determinants of acute cerebrovascular disease. According to the pathology of vascular origin and cytotoxicity. The former due to the destruction of the blood-brain barrier, capillary tight junction separation, plasma components to the surrounding extracellular matrix leakage caused. The latter is vascular endothelial cells, glial cells, nerve cell swelling, the mechanism of ischemia, decreased energy metabolism, Na pump disorders, sodium and water into the cells. Ischemic brain edema begins with cytotoxicity, followed by vasogenicity. However, it has recently been suggested that this may be related to the cell membrane barrier caused by free radical reaction. The free radicals produced by ischemia react with the polyunsaturated fatty acids that form the living membrane to produce peroxyesters, causing cell membrane disorders and damage to the blood-brain barrier membranes, which are predominantly composed of mitochondria and lysosomes. In addition, some people think that free radical reaction is due to ischemia to the brain tissue re-supply