Article Summary
程晓辉 徐学森 岳子勇 公维东 王楠.高碳酸血症对大鼠机械通气肺损伤时炎症因子和p38MAPK 表达的影响[J].现代生物医学进展英文版,2012,12(14):2605-2608.
高碳酸血症对大鼠机械通气肺损伤时炎症因子和p38MAPK 表达的影响
Effects of Hypercapnia on Expression of Inflammatory Cytokinesand p38MAPK in Ventilator-Induced Lung Injury in Rats
  
DOI:
中文关键词: 高碳酸血症  机械通气肺损伤  p38MAPK
英文关键词: Hypercapnia  Ventilator-induce lung injury  P38MAPK
基金项目:国家自然科学基金项目(30772085)
Author NameAffiliation
CHENG Xiao-hui, XU Xue-sen, YUE Zi-yong, GONG Wei-dong, WANG Nan 哈尔滨医科大学附属第二医院麻醉科黑龙江省麻醉与危重病学研究重点实验室
潍坊市妇幼保健院 
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中文摘要:
      目的:探讨高碳酸血症对大鼠机械通气性肺损伤(VILI)时炎症因子和p38MAPK 表达的影响。方法:健康雄性Wistar 大鼠 30 只,体重220~280g,采用随机数字表法,将大鼠随机分3 组(n=10):对照组(C 组)、机械通气肺损伤组(V 组)和高碳酸血症组 (H 组)。C 组保留自主呼吸,V 组和H 组行机械通气4 h。采用高气道压机械通气模式制备机械通气性肺损伤模型。H 组通过调整 吸入的CO2 浓度来维持动脉血PaCO2 分别为80~100mmHg。机械通气结束时,测定支气管肺泡灌洗液(BALF)中总蛋白、TNF-α 和巨噬细胞炎症蛋白-2(MIP-2)的浓度;取肺组织,测定湿干重比(W/D 比)、细胞间粘附分子(ICAM-1)和p38MAPK 蛋白的表达 水平以及p38MAPK 的活性,并观察病理学结果,进行肺损伤评分。结果:与C 组比较,V 组肺损伤评分、W/D 比、ICAM-1 表达水 平、BALF 中总蛋白浓度、TNF-α 和MIP-2 浓度和肺组织p38MAPK 活性升高,PaO2 降低(P<0.05);与V 组比较,H 组肺损伤评分、 W/D 比、ICAM-1 表达水平、BALF 中总蛋白浓度、TNF-α 和MIP-2 浓度和肺组织p38MAPK 活性降低,PaO2 升高(P<0.05)。结论: 高碳酸血症通过调节p38MAPK 的表达,从而抑制炎症反应减轻大鼠机械通气肺损伤。
英文摘要:
      Objective: To investigate the effects of hypercapnia on the inflammatory cytokines and p38MAPK in ventilator lung injury in rats. Methods: Thirty male Wistar rats weighting 250~280g were randomly divided into 3 groups (n=10 each):control group (group C),VILI group(group V), hypercapnia group(group H).A rat model of lung injury induced by ventilation with high peak inspiratory pressure(PIP). Parameter of ventilation: PIP=25cmH2O, PEEP=2cmH2O, the fraction of inspiratory O2 50% and adjusting the level of CO2 to maintained PaCO2 of group V and group H at 35~45mmHg and 80~100mmHg respectively. The rats were sacrificed by exsanguination 4h of mechanical ventilation and the lung tissues were removed for microscopic examination, lung wet to dry weight ratio(W/D), determination of ICMA-1(by immuno-histochemistry), p38 and phosphorylated p38(p-p38) expresstion (byWestern blotting) and determination of TNF-α, MIP-2 (by enzyme linked immunosorbent assay) and total of protein concentration in bronchoalveolar lavage fluid(BALF). Results: Compared with group C, the lung injury score, W/D ratio, TNF-α, MIP-2,total protein concentrations in BALF, ICAM-1 expression and p38MAPK activity in lung tissue were increased, PaO2 were decreased in groups V (P<0.05). Compared with group V, the lung injury score, W/D ratio, TNF-α, MIP-2, total protein concentrations in BALF, and MAD content, ICAM-1 expression and p38MAPK activity in lung tissue were decreased, PaO2 and were increased in group P (P<0.05). Conclusions: Hypercapnia attenuated ventilator-induce lung injury by regulating the expression of p-p38MAPK that inhibit the expression of inflammatory cytokines in rat lung tissues.
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