大鼠急性颅脑损伤后脑肿胀及钙镁离子的变化  

Changes in Ca and Mg Levels in Brain Tissue and Encephaledema after Acute Craniocerebral Injury in Rats

作　　者：李培建[1] 卢进发[2] 黄河玲[2] 曹雪滨[2] 古彩哲[2] 

机构地区：[1]解放军第二六一医院临床实验室,北京100094 [2]解放军第二五二医院实验动物中心,河北保定071000

出　　处：《实验动物科学》2007年第4期8-11,共4页Laboratory Animal Science

摘　　要：目的研究大鼠急性颅脑损伤后脑肿胀及钙镁离子的改变,以找出颅脑损伤后病情转化的规律,为临床治疗提供依据。方法大鼠40只随机分为4组,采用自由落体致大鼠脑挫裂伤,伤后122、44、8 h分别取材,观察脑肿胀及钙镁离子的变化。结果大鼠急性颅脑损伤后脑肿胀在24 h达到高峰,钙镁离子也有相应变化。结论急性颅脑损伤后脑肿胀的变化有一定的规律可循,产生外伤性脑肿胀的病理基础为脑血管扩张充血导致微循环障碍,救治急性颅脑损伤要重视预防微循环障碍,及时脱水,纠正缺血、缺氧。Objective To investigate changes in Ca （calcium） and Mg （magnesium） levels in brain and encephaledema after acute craniocerebral injury in the rats so as to provide the scientific basis for the clinical treatment. Methods The brain injury was developed by free falling body in 40 rats, and the rats were sacrificed by excess anaesthesia and the brain tissues were sampled respectively 12, 24, 48 hours after the brain injury. The pathological changes of the brain tissues were observed by macroscopy, microscopy, and electronic microscopy and Ca and Mg levels in brain were determined by atomic absorption spectrophotometry. Results Ca level in brain tissues was significantly increased 24, 48 hours after the brain injury as compared with the control group （ P 〈 0.05） and the elevation of Ca level at 24 hours after brain injury was the most notable, and Mg level was not significantly changeable. The brain edema extended to deep layer of white matter, obvious edema around the vessel, formation of platelet microthrombus in the micrangium, proliferation of the vascular endotheliocyte, and the luminal compression were revealed by microscopy and electronic microscopy. Conclusion The microcirculatory disturbance resulted from the cerebrovascular hemangiectasis and congestion was pathological basis of traumatic brain edema. Thus, the great attention should be paid to improving brain microcirculation in the treatment of head injury.

关 键 词：颅脑损伤 脑肿胀 钙镁离子变化 微循环障碍 

分 类 号：R151.2[医药卫生—营养与食品卫生学]