摘要
目的 研究预高温和缺血时轻度高温、亚低温对脑缺血再灌注损伤组织脂质过氧化和缺血脑组织病变的影响。方法 75只Wistar大鼠按不同脑温和缺血条件被随机分为生化组 (5组 ,n=7) 和病理组 (5组 ,n=8) ,采用Nagasawa脑缺血模型 ,观察脑缺血再灌注损伤组织超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)、还原型谷胱甘肽 (GSH)、丙二醛 (MDA)及缺血脑组织病理变化。结果 轻度高温加重常温脑缺血组织SOD、GSH的降低和MDA的增高 ,使GSH Px呈降低趋势 ,而亚低温相反 ;预高温对常温脑缺血各项指标影响不显著。轻度高温组脑缺血病理损伤最重 ,亚低温和预高温有改善脑缺血损伤的作用。结论 高温加重而亚低温抑制脑缺血损伤 ,分别与其增加或减少内源性抗氧化酶消耗、降低或增强缺血脑组织清除氧自由基的能力有关 ;预高温对缺血脑组织有保护作用 。
Objective To study the different effects of pre ischemic hyperthermia and intraischemic mild hyperthermia and mild hypothermia on lipid peroxidation and the patho histologic changes of the focal ischemia reperfused cerebral tissue.Methods Seventy five Wistar rats were randomly divided into two groups:biochemical group and pathological group.Each group was further divided into five subgroups(n=7 or n=8) according to different brain temperatures and different states of ischemia,respectively.Using the improved model of Nagasawa focal cerebral ischemia, the content of SOD,GSH Px,GSH,MDA and the pathologic changes of ischemia reperfused cerebral tissue were studied.Results Among the different groups,either the decline in SOD, GSH Px and GSH or the increase in MDA was greatest and the pathologic changes were most severe in the mild hyperthermia group.Pre hyperthermia and mild hypothermia could decline the degree of injury of the ischemic cerebral tissue.Mild hypothermia obviously alleviated all biochemical changes in hyperthermia group and normothermia group, whereas pre hyperthermia had no statistically significant effect.Conclusions Hyperthermia made the injury of cerebral ischemia worse,which was related to the increase in the consumption of endogenous antioxidant enzymes and the decrease in the clearance of free radicals in ischemic cerebral tissue,whereas the mild hypothermia decreased the degree of injury, which was related to the decrease in consumption of endogenous antioxidant enzymes and the increase in the clearance of free radicals in ischemic cerebral tissue.Pre hyperthermia had protective effect on ischemic cerebral tissue, but no relation to the decrease in the consumption of endogenous antioxidant enzymes and the increase in the clearance of free radicals in ischemic cerebral tissue could be observed.
出处
《中华老年心脑血管病杂志》
CAS
2002年第3期198-201,共4页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
广西壮族自治区卫生厅立项课题 (Z 2 0 0 0 15 )
