论文部分内容阅读
目的研究高容量血液滤过(HVHF)对内毒素诱导犬急性肺损伤(ALI)的治疗作用,并探讨其机制。方法选用健康犬16条,经中心静脉注入内毒素(LPS)650μg/kg诱导犬急性肺损伤模型,随机分为两组,对照组采用单纯机械通气+假治疗,治疗组采用机械通气+HVHF治疗。监测LPS注入后0h、成模时及HVHF治疗后4h动脉血气。采用放射免疫法测定HVHF治疗后1h、2h、4h循环血TNF-α、IL-6、IL-10的含量。采用RT-PCR法测定肺组织匀浆内TNF-α、IL-6、IL-10 mRNA表达。采用流式细胞仪测定肺组织匀浆内NF-(?)B活性。结果动物注入LPS后PaO_2和PaO_2/FiO_2下降,成模时PaO_2/FiO_2小于300。HVHF治疗后PaO_2、PaO_2/FiO_2呈轻度上升,同时点值明显高于治疗组(P＜0．01)。HVHF治疗1h治疗组循环血中TNF-α、IL-6、IL-10的浓度即有明显下降,同时点值低于对照组(P＜0．01)。HVHF治疗4h后,治疗组TNF-α．IL-6、IL-10mRNA的表达及NF-(?)B活性度均下降,低于对照组(P＜0．01)。结论HVHF能通过清除炎症介质．抑制NF-(?)B的活化,从而下调细胞因子的高表达和炎症反应,减轻ALI,为临床治疗ALI提供了一条新途径。
Objective To investigate the therapeutic effect of high-volume hemofiltration (HVHF) on endotoxin-induced acute lung injury (ALI) in dogs and its mechanism. Methods Sixteen healthy dogs were randomly divided into two groups. The rats in the control group were treated with mechanical ventilation alone or with sham. The rats in the treatment group were treated with mechanical ventilation + HVHF . Blood samples were taken at 0 h after LPS injection and at 4 h after HVHF treatment. The levels of TNF-α, IL-6 and IL-10 in the blood of 1h, 2h, 4h after HVHF treatment were measured by radioimmunoassay. The expression of TNF-α, IL-6 and IL-10 mRNA in lung homogenate was determined by RT-PCR. The activity of NF -? B in lung homogenate was determined by flow cytometry. Results The PaO_2 and PaO_2 / FiO_2 decreased after LPS injection, and PaO_2 / FiO_2 was less than 300 at the time of injection. After HVHF treatment PaO_2, PaO_2 / FiO_2 slightly increased, while the value was significantly higher than the treatment group (P <0.01). The concentration of TNF-α, IL-6 and IL-10 in the circulating blood of HVHF treatment group decreased significantly at 1 hour after treatment, and the value of HVHF was lower than that of the control group (P <0.01). After 4 hours of HVHF treatment, the treatment group TNF-α. The expression of IL-6, IL-10mRNA and the activity of NF -? B decreased, which was lower than that of the control group (P <0.01). Conclusion HVHF can eliminate inflammatory mediators. Inhibit the activation of NF -? B, thus downregulating the high expression of cytokines and inflammatory response, reduce ALI, for the clinical treatment of ALI provides a new way.