脑梗死合并肺部感染后血浆血栓调节蛋白与肿瘤坏死因子α的相关性

The Relationship between Serum Thrombomodulin and Tumor Necrosis Factor-α in Acute Cerebral Infarct with HAP

目的观察脑梗死合并医院内获得性肺炎患者血栓调节蛋白含量的变化及其与血浆肿瘤坏死因子的相关性,探讨脑梗死合并医院内获得性肺炎对脑梗死后内皮细胞损伤和凝血机制的影响。方法初发脑梗死患者分为单纯脑梗死组和脑梗死合并医院内获得性肺炎组,设立健康对照组。脑梗死发病后第1、3、5、7、14和21天分别采血。采用酶联免疫吸附法检测血栓调节蛋白水平,采用放射免疫法检测肿瘤坏死因子α水平。结果脑梗死合并医院内获得性肺炎后第7和14天血栓调节蛋白与单纯梗死组相比下降(P<0.05),21天与单纯梗死组比较无统计学差异但仍高于健康对照组。单纯脑梗死组与脑梗死合并医院内获得性肺炎组肿瘤坏死因子α水平第1天无统计学差异,两组均高于健康对照组。脑梗死合并医院内获得性肺炎发生第7和14天肿瘤坏死因子α明显增高,高于单纯脑梗死组(P<0.05);21天虽然医院内获得性肺炎已控制肿瘤坏死因子α仍高于单纯梗死组(P<0.05)。脑梗死合并医院内获得性肺炎组血栓调节蛋白与肿瘤坏死因子α有相关性。随着肿瘤坏死因子α增高,血栓调节蛋白有下降趋势,两者相关关系以Gompertz曲线拟合满意,在高浓度肿瘤坏死因子α时血栓调节蛋白降低较快,而低浓度肿瘤坏死因子α时血栓调节蛋白降低较慢。结论脑梗死合并医院内获得性肺炎后血浆肿瘤坏死因子α增高,可能导致脑血管内皮细胞的损伤和抗凝机制的抑制,表现为血栓调节蛋白的下调,这可能是获得性肺炎加重缺血性脑损伤的机制之一。

Aim To observe the change of thrombomodulin and its relationship with tumor necrosis factor-α （TNF-α）in acute cerebral infarct with hospital acquired pneumonia （HAP）. Methods The patients with acute cerebral infarct were divided into pure infarct group （ n = 24）, and acute infarct with HAP group （ n = 16）, compared with normal control group（ n = 13 ）. The serum samples were obtained from 1 d to 21 d after infarct, The serum level of thrombomodulin and TNF-α were examined by enzyme-linked immunosorbent assay（ELISA） method and radioimmunoassay respectively. Results The serum levels of thrombomodulin of acute infarct with HAP group were significantly lower than those of pure infarct group in the first week and 14 d after infarct （P〈0.05）, with similar resuh at 21 d. The serum levels of TNF-α of acute infarct with HAP group were significantly higher than those of pure infarct group from the first week to 21 d after infarct （ P 〈 0.05）, although HAP had been prohibited in 21 d. In the group of acute infarct with HAP the serum levels of thrombomodulin were related inversely with that of TNF-α, The relationship between thrombomodulin and TNF-α compromised with Gompertz curve, Conclusions It＇ s possible that the increase of serum TNF-α in acute infarct with HAP may injury the endotheliocyte of brain vessel and prohibited the anticoagulative system, presenting with downregulation of the level of serum thrombomodulin.