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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 ,未能肯定此作用与内源性抗氧化酶消耗减少和缺血脑组织清除氧自由基的能力增强有关
Objective To study the effects of mild hypothermia and mild hypothermia on lipid peroxidation and ischemic brain damage in rats with preconditioning and ischemia. Methods 75 Wistar rats were randomly divided into biochemical group (n = 5) and pathological group (n = 8) according to different conditions of cerebral ischemia. Nagasawa cerebral ischemia model was used to observe cerebral ischemia The changes of superoxide dismutase (SOD), glutathione peroxidase (GSH Px), glutathione (GSH), malondialdehyde (MDA) and pathological changes in ischemic brain tissue were observed after reperfusion injury. Results Mild hyperthermia aggravated the decrease of SOD, GSH and MDA in normal temperature ischemic tissue, which decreased the GSH Px, but the opposite of mild hypothermia. The effect of pre-high temperature on indexes of normal temperature was not significant. Mild hyperthermia group, the most severe ischemic pathological damage, mild hypothermia and pre-hyperthermia have a role in improving cerebral ischemia. Conclusions High temperature exacerbated hypothermia inhibits cerebral ischemic injury, which is related to its ability to increase or decrease the consumption of endogenous antioxidant enzymes and reduce or enhance the ability of oxygen free radicals to scavenge ischemic brain tissue respectively. Pre-hyperthermia has a protective effect on ischemic brain tissue , Failed to confirm that this effect is associated with reduced endogenous antioxidant enzyme consumption and increased ability of brain tissue to scavenge oxygen free radicals