TNF-α及IL-8在机械通气治疗ARDS动物模型中表达

Expression of INF-α and DL - 8 in a animal model of acute respiratory distress syndrome during mechanical ventilation

目的探讨肿瘤坏死因子-α(TNF-α)和白细胞介素-8(IL-8)在呼吸机治疗急性呼吸窘迫综合征(ARDS)动物模型中的表达。方法选用12只大白兔,制作ARDS模型,将模型随机分为两组:低潮气量通气治疗组(A,n=6,VT=6 mg/kg)和正常通气治疗组(B,n=6,VT=10 mg/kg),分别于肺通气前、通气120 min后收集支气管肺泡灌洗液(BALF)检测TNF-α及IL-8的浓度;采集肺通气前(T0)、通气后(T1)、通气30 min(T2)及60 min (T3),通气后120 min(T4)血清,采用酶联免疫法(ELISA)检测TNF-α及IL-8的浓度,监测两组血气变化。结果ARDS建立后,BALF、血清中TNF-α及IL-8表达明显升高;机械通气治疗后,BALF、血清TNF-α及IL-8表达较通气前明显下降(P<0.01),但B组于60及120min血清TNF-α及IL-8表达上调,与A组比较明显升高(P<0.01)。结论低潮气量通气治疗ARDS动物模型能够减轻炎症诱发细胞因子的释放,减轻机械通气相关性肺损伤。

Objective To study the expression of TNF-αand IL - 8 in an animal model of acute respiratory distress syndrome during treatment of mechanical ventilation. Methods Model of ARDS was established in twelve in healthy rabbits. The animal models of ARDS were randomized into two groups ： ventilation at low udal volume group （group A, n = 6, VT = 6 ml/kg） and ventilation at normal tidal volume group （group B, n = 6, VT = 10 ml/kg）. The BALF were obtained before ventilation and 120 min after ventilation in both groups. The serums were obtained before ventilation（T0）, at ventilation（T1）, 30 min after ventilation（T2）, 60 rain after ventilation（T3） and 120 rain after ventilation（T4） in both groups. The concentrations of TNF-α and IL- 8 in BALF and sera were measured with ELISA. Artery blood gas were measured in both groups. Results The concentrations of TNF - αand IL - 8 in BALF and serum increased in both groups after establishment of the model of ARDS（ P 〈 0.01 ）. After ventilation, the concentrations of serum TNF-α and IL - 8 of serums significantly decreased in both groups（ P 〈 0.01）. The concentrations of serum TNF-α and IL- 8 of serums increased in 60 min after ventilation（T3） and 120 min after ventilation （T4） in B group. The concentations of serum TNF - α and IL - 8 significantly higher than those of A group at the same time（ P 〈 0.01 ）. Conclusion Low tidal volume ventilation can decrease cytokine release and can alleviate ventilator-induced lung injury （VILI） in animal models of ARDS.