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目的 :探讨亚低温能否抑制内毒素 (L PS)介导的小鼠细胞因子与粘附分子的表达与释放 ,从而阻止多器官功能障碍综合征 (MODS)的发生。方法 :96只小鼠随机分成内毒素、亚低温、保温及对照 4组 ,采用放射免疫法 ,分别于注射 L PS后 1、2和 4小时进行血清肿瘤坏死因子 α(TNFα)测定 ,并用免疫组化法检测 4组动物 (4小时 )肝、肺血管内皮细胞上细胞间粘附分子 1(ICAM 1)的表达情况。结果 :亚低温组 1、2和 4小时的 TNFα含量显著低于内毒素组 (P均 <0 .0 1) ,而保温组与内毒素组无显著差别 (P均 >0 .0 5 ) ;亚低温组与保温组在 1和 2小时有显著差异 (P<0 .0 1和 P<0 .0 5 ) ,但 4小时未见明显差异 (P>0 .0 5 )。免疫组化显示低温组肝及肺微血管内皮细胞周围的 ICAM 1组化染带呈弱阳性 ,内毒素与保温组呈强阳性表达。结论 :亚低温有显著抑制全身性炎症反应小鼠 TNFα与 ICAM 1的表达与释放作用。提示亚低温可考虑作为防治全身炎症反应综合征 (SIRS)或 MODS的新措施
Objective: To investigate whether mild hypothermia can inhibit the expression of LPS - induced cytokines and adhesion molecules in mice and prevent the occurrence of multiple organ dysfunction syndrome (MODS). Methods: Ninety-six mice were randomly divided into four groups: endotoxin, mild hypothermia, heat preservation and control group. The levels of tumor necrosis factor alpha (TNFα) were determined by radioimmunoassay at 1, 2 and 4 hours after LPS injection, The expression of intercellular adhesion molecule 1 (ICAM 1) in liver and pulmonary vascular endothelial cells was detected by histochemistry in 4 groups of animals (4 hours). Results: The levels of TNFα at 1, 2 and 4 hours in the mild hypothermia group were significantly lower than those in the endotoxin group (all P <0.01), while there was no significant difference between the heat preservation group and the endotoxin group (P> 0.05). There was a significant difference between the hypothermia group and the heat preservation group at 1 and 2 hours (P <0. 01 and P <0. 05), but no significant difference was found after 4 hours (P> 0.05). Immunohistochemistry showed that ICAM 1 staining bands in the liver and lung microvascular endothelial cells of the hypothermia group were weakly positive, while that of the endotoxin and the heat preservation group was strongly positive. Conclusion: Mild hypothermia can significantly inhibit the expression and release of TNFα and ICAM 1 in mice with systemic inflammatory response. Suggesting that hypothermia may be considered as a new measure for the prevention and treatment of systemic inflammatory response syndrome (SIRS) or MODS