关键词:肠缺血再灌注;内毒素;抗体;CD14;肿瘤坏死因子;多器官功能障碍综合征
【摘要】 目的 探讨肠缺血再灌注损伤(I/R)对内毒素的增敏作用及其机制。方法 大鼠肠系膜上动脉阻断45min后松夹进行再灌注,静脉注射低剂量内毒素(LPS,1.5 mg/kg)。观察动物多脏器功能指标及体外诱生肿瘤坏死因子(TNF)的改变。结果 I/R+LPS组显著加重全身血流动力学异常改变和肝、肺、肠等器官功能损害(P<0.01)。而单纯LPS组或I/R组上述指标改变较轻或无明显异常。体外试验显示,当LPS刺激浓度≤10 ng/ml时,抗CD14单抗可显著抑制全血TNF的诱生(P<0.05~0.01),且I/R组抗CD14单抗对LPS诱导TNF的抑制率明显高于伤前值或假手术组(P<0.05~0.01)。结论 I/R可显著提高机体对LPS攻击的敏感性,其机理与体内CD14依赖途径的作用增强有关。
The effect of intestinal ischemia/reperfusion on increased sensitivity to endotoxin and its potential mechanism
YAO Yongming,YU Yan,CHENJinsong,et al.Burn Institute,304 th Hospital of People's Liberation Army,Beijing 100037
【 Abstract 】 Objective To investigate the effect ofintestinal ischemia/reperfusion injury (I/R)on increased sensitivity to endotoxin and itspotential mechanism(s).Methods Sprague-Dawley rats underwent 45 minutes of superiormesenteric artery occlusion followed by reperfusion.Twelve hours afterreperfusion,endotoxin (Escherichia coli LPS,1.5 mg/kg)was injected intravenously and ratswere killed 12 hours later for measurement of organ function parameters.Also,in vitrostudy was performed to determine LPS-induced tumor necrosis factor (TNF)release in wholeblood.Results LPS injection after I/R resulted in marked hemodynamic dysfunctionand multiple organ damage(P<0.01) ......
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