摘要
目的 研究局灶亚低温治疗对创伤性脑损伤大鼠脑组织中水含量、cNOS和iNOS含量的影响，以探讨局灶亚低温对创伤性脑损伤的治疗作用及可能的脑保护机制。方法 采用自由落体打击装置制备大鼠创伤性脑损伤模型，于伤后30min开始以25℃水进行局灶亚低温治疗（31～32℃），维持3h；伤后1、3、5、7d处死留取脑组织标本，采用干湿重法测伤灶脑组织含水量，以分光光度法检测脑组织中cNOS和iNOS活性含量。结果 与外伤模型组相比，局灶亚低温组伤灶脑组织水含量明显降低（P〈0．05）；脑外伤后1、3、5、7d伤灶脑组织中cNOS含量呈进行性下降，第3天开始脑组织中iNOS含量明显增加，第7天达高峰；经局灶亚低温治疗后，伤灶脑组织中cNOS下降幅度明显受抑，第5、7天更显著；同时抑制了第3天脑组织中iNOS的增高，第5，7天更显著。结论 局灶亚低温治疗能明显减轻伤灶脑水肿；调节NO的表达，是脑保护作用的机制之一。
Objective To explore the effects of focal moderate hypothermia on brain edema and the alternations in nitric oxide synthase （NOS） activities folIowing traumatic brain injury （TBI） in rats. Method Rats were underwent severe lateral controlled cortical impact brain injury. Thirty minutes after TBI, focal moderate hypothermie treatment was implemented by the copper pipe with 25℃ water. Brain temperature was reduced to 31 ～32℃ within 20～30 minutes, and maintained for 3 hours. Rats were decapitated 1 day, 3 days, 5 days, 7 days after injury, The percentage of water in the injured parietal cerebral cortex, as well as cNOS and iNOS activities were measured. Results In normothermic rats, significant brain edema was deteeted at 1,3 days after TBI in the iniured parietal cerebral cortex, and began to decline at 5 and 7 days. The brain edema was significantly reduced with posttraumatic focal moderate hypothermia. In normothermic rats, the enzymatic activity of eNOS was significantly decreased at 1, 3, 5 and 7days after TBI compared with the sham injured group. The cNOS activity was preserved at 1, 3, 5 and 7 days after focal hypothermie treatment. In normothermic rats, the enzymatic activity of iNOS was significantly increased at the 3rd day, and most robustly increased at the 7th day. Focal hypothermia also significantly reduced the rise in iNOS activity at 3, 5 and 7 days after TBI. Conclusion Focal moderate hypothermia can reduce traumatic brain edema significantly. To regulate NOS activity is one of its mechanisms.
出处
《中国耳鼻咽喉颅底外科杂志》
CAS
2006年第5期339-342,共4页
Chinese Journal of Otorhinolaryngology-skull Base Surgery
