论文部分内容阅读
在全世界范围内,创伤性颅脑损伤(TBI)的高死残率在现代社会中严重威胁着人类生命及生活质量。颅脑创伤后可导致无数的代谢和生化过程,其机制复杂,兴奋性氨基酸的释放、炎性反应、氧自由基反应、脑缺血、Ca2+超载、缺血再灌注损害等病理性损害又进一步加重了脑损伤。多项药物治疗颅脑创伤的临床多中心随机双盲研究中包括激素、自由基清除剂、钙拮抗剂、谷氨酸(Glu)受体拮抗剂、生长激素/胰岛素样生长因子、缓激肽拮抗剂、抗癫痫药等,迄今为止还没有一种外源性药物被证实对TBI有确切的疗效[1]。随着对颅脑损伤的继发性
Across the world, the high rate of death from traumatic brain injury (TBI) is a serious threat to human life and quality of life in modern society. Cranial trauma can lead to numerous metabolic and biochemical processes, its mechanism is complex, the release of excitatory amino acids, inflammatory reactions, oxygen free radical reactions, cerebral ischemia, Ca2 overload, ischemia-reperfusion injury and other pathological damage further Aggravate brain damage. Clinical multicenter, randomized, double-blind studies of multiple drug treatments for traumatic brain injury include hormones, free radical scavengers, calcium antagonists, glutamate receptor antagonists, growth hormone / insulin-like growth factor, Antagonists, antiepileptic drugs, etc., so far there is no exogenous drugs proved to have the exact effect of TBI [1]. With secondary to brain injury