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作 者:李欣[1] 荆小莉[1] 熊艳[1] 蔺际龚[1] 李玉杰[1] 马中富[1] 廖晓星[1]
机构地区:[1]中山大学附属第一医院急诊科,广州510080
出 处:《中华急诊医学杂志》2006年第1期19-22,共4页Chinese Journal of Emergency Medicine
基 金:广州市重大科技攻关项目(2004Z3E0381)
摘 要:目的观察心搏骤停患者经心肺脑复苏(CPCR)后核因子κB(NFκB)活性和肿瘤坏死因子α(TNFα)水平的变化及意义。方法以电泳迁移率变动分析法(EMSA)检测外周血单个核细胞的NFκB活性,放射免疫法测定血清TNFα水平。结果NFκB活性、TNFα水平和APACHEⅡ评分在复苏后多脏器功能障碍综合征(PRMODS)组和死亡组分别明显高于非PRMODS组和存活组(P<0.05);NFκB活性、TNFα水平和APACHEⅡ评分均呈正相关(P<0.05)。结论心搏骤停和CPCR过程可以使NFκB激活、TNFα表达增加,这对PRMODS的发生、病情轻重具有重要决定作用。Objective To study the change and role of nuclear factor-kappa B (NF-kB) activity and tumor necrosis factor-alpha (TNF-α) level in patients with cardiac arrest after cardiopulmonary-cerebral resuscitation (CPCR). Methods The NF-kB activity in monocytes was measured by dectrophoretic mobility shift assays (EMSA) and the level of TNF-α in serum was measured by radioimmunoassay. Results The NF-kB activity, TNF-α level and APACHE Ⅱ score in both post-resuscitation multiple organ dysfunction syndrome (PR-MODS) group and death group were higher than those in nonPR-MODS group and survival group ( P 〈 0.05). There was a positive correlation among NF-kB activity, TNF-α level and APACHE Ⅱ score ( P 〈 0.05). Conclusion Cardiac arrest and the CPCR procedure can activate NF-kB and then induce high expression of TNF-α, NF-kB is therefore a good marker for the occurrence and severity of PR-MODS.
关 键 词:心肺脑复苏 复苏 多脏器功能障碍综合征
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