摘要
一氧化氮（NO）在原代神经元培养中介导谷氨酸的兴奋性毒性，为探讨脑外伤后NO的变化及其对脑水肿的影响。建立大鼠液压脑外伤模型的基础上，运用生化及放免方法测定脑外伤后不同时期NO，环磷酸鸟苷（cGMP），脑组织含水量的变化，同时进行病理学检查。结果：脑外伤后血浆NO、脑组织NO及cGMP含量、脑组织含水量均升高，P＜0．05。其中血浆NO从5．141±0．449μM升高至10.274±1．193μM，脑组织NO从0.431±0.051nmol／mgpro升高至0.973±0.131nmol／mgpro，脑组织cGMP从1．452±0.383pmol／mgpro升高至3．398±1．109pmol／mgpro，脑组织含水量从76.93±0．434％升高至81．25±0．158％，P＜0．05。脑组织含水量与脑组织NO、cGMP及血浆NO之间呈正相关关系，P＜0．05。病理检查示NO升高伴随着脑组织的损伤。本文提示：脑外伤后NO可能部分参与了外伤后脑水肿的发生。
Nitric oxide (NO) has been found as a mediator of glutamate exitotoxicity in primary neuronal cultures.To study the changes of NO and its response to brain edema, the brain injury model of fluid percussion was produced in rats. During different time after brain injury, something was investigated by biochemistry and radiommunoassay method, such as the levels of NO, cyclic guanosine monophosphate(cGMP)and water content in brain tissue, meanwhile the histopathology was examined. The results showed NO in plasma, NO, cGMP and water content in brain tissue were significantly increased after brain injury (P<0. 05). The level of NO in plasma raised from 5. 141 ±0. 449μM to 10. 274±1. 193μM,the level of NO in brain tissue raised from 0. 431 ±0.051nmol/mg pro to 0. 973±0. 131 nmol/mg pro, the level of cGMP in brain tissue raised from 1. 452±0. 383pmol/mg pro to 3. 398±1. 109 pmol/mg pro, and the level of water content in brain tissue raised from 76. 93±0. 434 % to 81. 25 ±0. 158% (P<0. 05). There was positive correlation among NO, cGMP and water content (P< 0. 05 ). The histopathology showed that the increased NO was associated with the cerebral tissue damage. These findings suggest that NO may partially be involved in the pathogenetic mechanisms of brain edema after brain injury.
出处
《上海医学》
CAS
CSCD
北大核心
1997年第3期133-135,共3页
Shanghai Medical Journal
关键词
脑外伤
一氧化氮
脑水肿
Brain injury
Nitric oxide
Brain edema
