摘要
目的:建立机械通气相关性肺损伤模型兔肺组织,观察TNF-α在机械通气相关性肺损伤模型兔肺组织中TNF-α的变化规律,探讨乌司他丁对呼吸机所致肺损伤(ventilator-induced lung injury,VILI)的治疗机制是否与抑制TNF-α的活化有关。方法:采用大潮气量通气建立呼吸机相关肺损伤兔模型,模型成立后30、60、120、180、240 min,抽取动脉血作血气分析,采用ELISA法检测血清肺组织中TNF-α的含量,采用HE染色观察肺组织病理变化,运用Real-time PCR、Western Blot检测肺组织中TNF-αRNA、蛋白的表达。结果:家兔在大潮气量机械通气后,随着时间的增加血清中、肺组织中TNF-α表达显著增加,而采呼吸机相关性肺损伤模型兔在使用乌司他丁干预后,动脉血中的PaO_2较前有所回升,血清与肺组织中TNF-αm RNA与蛋白的表达同大潮气量组相比有明显著上升(P<0.05)。结论:乌司他丁对呼吸机相关性肺损伤有保护作用,其机制可能是通过下调TNF-α的表达,抑制炎症反应来实现的。
Objective： The establishment of ventilator induced lung injury in a rabbit model of lung tissue, to observe the changes of TNF- α in mechanical ventilation induced lung injury model of rabbit lung tissue alpha, to explore the therapeutic mechanism of Ulinastatin on VILI and TNF-α .Method： The injury rabbit model of high tidal volume ventilation was established, after 30, 60, 120, 180 and 240 min, arterial blood for blood gas analysis.TNF-α in serumwere measured by ELISA.The pathological changes of lung tissue were observed by HE staining.The expression of TNF-α RNA and protein in hung tissue was detected by PCR Real-time and Blot Western.Result： After mechanical ventilation, the expression of TNF-α in serum and lung tissue increased significantly.Ulinastatin interred ventilator induced lung injury model in rabbits and rabbit arterial blood PaO2 increased, in serum and lung tissue TNF- α expression were compared with those of the earlier high tidal volume group improved significantly （ P〈0.05 ） .Conclusion： Ulinastatin on ventilator induced lung injury has a protective effect, he mechanism may be by down regulating the expression of TNF- α , inhibit inflammatory reaction to achieve.
出处
《中国医学创新》
CAS
2016年第32期18-21,共4页
Medical Innovation of China
基金
福州市科技计划项目(2011-S-67-6)
