实验性大鼠弥漫性脑损伤后GFAP、NO和ET的变化研究

发布时间：2018-10-10 11:12

【摘要】：背景和目的创伤性脑损伤(Traumatic brain injury，TBI)有较高发生率，是导致创伤病人伤残及死亡的主要原因，严重危害人类健康，给社会和家庭带来沉重负担。弥漫性脑损伤(Diffuse brain injury，DBI)在TBI中占有重要地位，流行病学调查显示DBI占交通伤后重型脑创伤的73％。长期以来，DBI被认为是脑损伤后持续性昏迷及严重神经功能障碍的主要原因，有人统计创伤性昏迷病人资料发现有55％重度脑创伤病人存在DBI。DBI后可诱发系列病理生理改变(如脑血管自主调节功能紊乱、血脑屏障通透增加、脑组织缺血、颅内压增高等)、脑组织各种物质(如氧自由基、钙离子、兴奋性氨基酸、炎性细胞因子、电解质等)代谢紊乱及细胞凋亡等，造成脑组织继发损害，进一步加重病人脑损伤程度。目前对DBI的研究逐渐深入，但其机理尚未完全阐明，限制了治疗学的发展。研究DBI发病机制及其伤后病理生理变化、探索行之有效的脑保护治疗途径，将有助于提高病人的生存率及生存质量。我们改进了Marmarou法制作大鼠弥漫性脑损伤模型，，利用该模型观察损伤后脑组织的病理变化，检测反应性星形细胞(astrocyte，Ast)胶质纤维酸性蛋白(glial fibrillary acidic protein，GFAP)表达变化，并研究一氧化氮(nitric oxide，NO)和内皮素(endothlin，ET)在大鼠创伤脑组织中不同时间含量的变化规律，以探讨颅脑损伤的病理机制，进一步阐明三者在颅脑损伤后病理生理变化中的作用，为临床治疗脑损伤提供实验基础。方法 1、建立弥漫性脑损伤动物模型：采用Marmarou方法改良制作大鼠DBI模型。同时建立对照组进行对照比较。
[Abstract]:Background and objective traumatic brain injury (Traumatic brain injury,TBI) has a high incidence and is the main cause of disability and death of traumatic brain injury patients, which seriously endangers human health. It puts a heavy burden on society and families. Diffuse brain injury (Diffuse brain injury,DBI) plays an important role in TBI. Epidemiological investigation shows that DBI accounts for 73% of severe brain injury after traffic injury. DBI has long been considered to be the main cause of persistent coma and severe neurological dysfunction after brain injury. Some statistics showed that 55% of the patients with severe brain trauma had DBI.DBI, which could induce a series of pathophysiological changes (such as cerebral vascular autonomic regulatory dysfunction, increased blood-brain barrier permeability, cerebral ischemia. Various substances (such as oxygen free radicals, calcium ions, excitatory amino acids, inflammatory cytokines, electrolytes, etc.) metabolic disorders and apoptosis, etc. The degree of brain injury was further aggravated. At present, the research on DBI has gradually deepened, but its mechanism has not been fully elucidated, which limits the development of therapeutics. To study the pathogenesis of DBI and its pathophysiological changes after injury and to explore an effective way of brain protection therapy will help to improve the survival rate and quality of life of patients. We improved the Marmarou method to make the model of diffuse brain injury in rats. The pathological changes of brain tissue and the expression of glial fibrillary acidic protein (glial fibrillary acidic protein,GFAP) in reactive astrocytes (astrocyte,Ast) were observed by using the model. The changes of the contents of nitric oxide (nitric oxide,NO) and endothelin (endothlin,ET) in traumatic brain tissue of rats at different time were studied in order to explore the pathophysiological mechanism of traumatic brain injury and to elucidate the role of them in the pathophysiological changes after traumatic brain injury. To provide experimental basis for clinical treatment of brain injury. Methods 1. The animal model of diffuse brain injury was established. Marmarou method was used to improve the DBI model of rats. At the same time, the control group was established for comparison.
【学位授予单位】：郑州大学
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R361

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