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作 者:赵旭明[1] 刘励军[1] 周保纯[1] 肖盐[1]
出 处:《岭南急诊医学杂志》2009年第1期1-3,共3页Lingnan Journal of Emergency Medicine
基 金:江苏省教育厅"211"工程资助项目(No.R2317054)
摘 要:目的:研究心跳骤停大鼠内毒素受体的变化及亚低温对其影响。方法:建立大鼠心跳骤停模型,SD大鼠24只,随机分为3组:对照组、常规心肺复苏组、亚低温心肺复苏组,每组8只;三组大鼠分别在手术或复苏后24 h静脉注射3 mg/Kg LPS;并于手术或复苏后6 h、12 h、24 h,及注射LPS后1.5 h、3 h、6 h静脉取血;采用ELISA法,测定血浆可溶性内毒素受体CD14(sCD14)、肿瘤坏死因子α(TNF-α)含量;免疫组织化学法测定注射LPS后6 h左肺肺泡及肺间质巨噬细胞表面内毒素受体CD14(mCD14)蛋白表达;观察肺组织病理改变。结果:与对照组比较,复苏组在复苏和注射LPS后血浆sCD14水平明显升高,但亚低温组低于常规组(P<0.05);注射LPS后,各组TNF-α水平均增高,且与sCD14水平成正相关(r=0.92,P<0.01);常规组肺泡巨噬细胞mCD14表达明显高于亚低温组(P<0.01);常规组肺损伤评分也大于亚低温组(P<0.05)。结论:心肺复苏后大鼠存在内毒素受体的上调,伴随着对内毒素敏感性的增强;亚低温对其有抑制作用,减轻复苏后内毒素对肺的损害。Objective:To investigate the change of endotoxin receptor in cardiac arrest rat and the effect of mild hypothermia on the change.Methods:After setting up cardiac arrest model in rats,24 animals were randomly divided into control group(S group),routine resuscitation group(C group) and mild hypothermia resuscitation group(M group),(n=8,per group).All animals were injected 3 mg/kg LPS at 24 h after operation or after CPR.In three groups,the contents of sCD14 and TNF-αin the plasma were determined by enzyme immunoassay method at 6 h,12 h,24 h after CPR or operation,and then at 1.5 h,3 h,6 h after injection of LPS.The expression of mCD14 protein in alveolar macrophage(AM)and interstitial macrophage were determined by immunohistochemistry.Pathological observation were observed in the right lung.Results:Contrast to S group,the contents of sCD14 in other groups increased after CPR and injection of LPS,but M group was less than C group(P<0.05).After injection of LPS,the contents of TNF-αin all the groups increased.Furthermore,it was direct correlation between the contents of TNF-αand sCD14(P<0.01).The expression of AM mCD14 in C group was more than in M group(P<0.01).The ALI score was lower in group M.Conclusion:The expression of endotoxin receptor in cardiac arrest rat increased after CPR, meanwhile,enhanced sensitivity to the subsequent LPS challenge.But mild hypothermia could inhibit the increase, and mitigate the lung injury of LPS after CPR.
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