脑梗死体积及神经功能缺损程度与血清铁蛋白、肿瘤坏死因子的关系

Relation of neurologic impairment and volum of cerebral infarction with serum ferritin and tumor necrosis factor

目的:探讨血清铁蛋白(serumferritin,SF),肿瘤坏死因子(tumotnectosisfactor,TNF)与自由基在脑梗死患者血清中的变化与患者梗死体积及神经功能缺损的关系,为脑梗死的康复干预提供参考数据。方法:84例脑梗死患者为2002-03/10大连市友谊医院收治,年龄32～75岁,在发病48h内采用放射免疫分析法检测了84例脑梗死患者及30例同期门诊体检健康对照组的血清SF,TNF和自由基水平的变化。结果:脑梗死患者急性期血清SF,TNF,超氧化物歧化酶,丙二醛及皮质醇水平,脑梗死组数据分别为:(96.33±53.49),(2.16±0.18)μmol/L,(114.84±14.55),(17.16±16.28),(253.25±97.93)mg/L,对照组以上指标分别为(46.58±53.49),(0.93±0.16)μmol/L,(94.37±8.79),(125.01±85.77),(125.01±85.77)mg/L,两组比较差异均有非常显著性意义(P<0.01)。且不同梗死体积,不同神经功能损伤程度时上述各项指标差异存在显著性意义。结论:SF的升高可能是脑梗死发病的独立危险因素,且参与了脑梗死后的脑组织病理损伤过程,SF浓度越高,脑梗死体积越大,神经功能缺损评分越高。TNF在脑梗死的发病机制中也起了重要作用,它们均可促进自由基的释放,加剧缺血后脑损伤,

AIM:To observe the changes of serum ferritin(SF),tumor mecrosis factor(TNF) and free radicals in serum of patients with acute cerebral ischemia and the relation with neurologic impairment and volum of cerebral infarction in order to provide data for rehabilitation of cerebral infarction. METHODS:Radioimmunoassay was used to measure SF,TNF and free radicals in 84 patients with cerebral infarction selected from Dalian Youyi Hospital,32-75 years of age, and in 30 normal controls after health examination at the same time. RESULTS:The SF, TNF superoxide dismutase(SOD),malondialdchyde(MDA),and cortisol levels of patients at the acute stage were (96.33 ±53.49) μmol/L,(2.16±0.18) μmol/L,(114.84±14.55) mg/L,(17.16±16.28) mg/L,(253.25±97.93) mg/L,and(46.58 ±53.49) μmol/L,(0.93±0.16) μmol/L,(94.37±8.79) mg/L,(125.01±85.77) mg/L,(125.01±85.77) mg/L for the controls.There was significant difference between the two groups(P< 0.01).There was significant difference in the mentioned indexes at different infarction volum,different neurologic impairment degree. CONCLUSION:The increase of SF may be the independent risk factor for episode of cerebral infarction and its also participates in the damage of brain tissue.TNF plays an important role in the pathogenesis of cerebral infarction.They can promote the produce of free radicals to aggravate the damage of the brain tissue.