脑出血继发性神经损伤机制的研究

Mechanism Study of Secondary Nerve injury of Intracerebral Hemorrhage

脑出血后血肿周围脑组织存在继发性脑损伤,其病理机制十分复杂。最近研究表明,脑出血后血肿周围存在水肿形成和继发性缺血损伤区,脑出血后血肿周围缺血是引起脑水肿的主要原因之一;脑出血后血肿本身释放的毒性物质如凝血酶、血红蛋白等是导致神经细胞坏死、脑组织缺血、水肿等病理变化的重要化学刺激物;炎性反应在脑出血后血肿周围继发性脑组织损伤中起着十分重要的作用;另外,细胞凋亡、补体系统激活、细胞色素C释放、自由基反应增强等均参与了脑出血后神经细胞损伤。

The periphery tissue of hematoncus resulting from i ntracerebral hemorrhage often has secondary brain injury,of which the patholog ical mechanism is very complex.Recent studies showed that there are area of edematization and secondary ischemic injury around hematoncus after intra cerebral hemorrhage,among which the ischemia is the main cause resulting i n cerebral edema.Hematoncus can release some poisonous materials such as thromb ase,hemoglobin and so on,which are the important chemical stimulus resultin g in some pathological changes including neurocyte necrosis,brain tissue isch emia,edema and so on.Inflammatory reaction plays an important role in th e secondary brain injury around hematoncus after intracerebral hemorrhage.Besi des that,some other factors also participated the nerve injury after intracere bral hemorrhage including cell apoptosis,activation of complement system,re leasing of cytochrome C,increased free radical reaction and so on.