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1.
Many studies have suggestedthat high volumeventilation has the capable of inducing a completeinflammatory response by sti mulating the produc-tion of cytokines and chemokines that in turn at-tract and activate neutrophils and recruit ment intothe lung which caused the lung injury[1 ,2],that is“ventilation-induced lung injury ( VILI)”. It hasbeen the vital complications in pateints withbreathing machine therapeutics such as ARDS,MOSF,SIRS and so on. Recent investigation hassuggested the…  相似文献   

2.
Acute respiratory distress syndrome (ARDS) is a life threatening respiratory failure due to lung injury from a variety of precipitants.Mechanical ventilation (MV) is the foundation in the supportive management of patients with ARDS.1 However,it is associated with several complications,such as increased risk of pneumonia and development of lung injury.The improved understanding of ARDS and complications from MV has been considered important in designing lung-protective ventilatory strategies aimed at attenuating or preventing organ dysfunction and improving outcomes.  相似文献   

3.
Mechanical ventilation (MV) may aggravate lung injury induced by a variety of injuries, including intratracheal hydrochloric acid instillation, intratracheal lipopolysaccharide (LPS) instillation with or without concurrent saline lavage, intravenous LPS, or intravenous oleic acid. However, the mechanism for this detrimental effect of MV is unclear. The purpose of the present study was to determine the effect of MV on lung injury induced by minimal LPS-instillation and on the LPS receptor CD14 in the lung.  相似文献   

4.
Background Animal models that demonstrate changes of renal function in response to acute lung injury (ALI) and mechanical ventilation (MV) are few. The present study was performed to examine the effect of ALI induced by oleic acid (OA) in combination with conventional MV strategy on renal function in piglets.
Methods Twelve Chinese mini-piglets were randomly divided into two groups: the OA group (n=6), animals were ventilated with a conventional MV strategy of 12 ml/kg and suffered an ALI induced by administration of OA, and the control group (n=6), animals were ventilated with a protective MV strategy of 6 ml/kg and received the same amount of sterile saline.
Results Six hours after OA injection a severe lung injury and a mild-moderate degree of renal histopathological injury were seen, while no apparent histological abnormalities were observed in the control group. Although we observed an increase in the plasma concentrations of creatinine and urea after ALI, there was no significant difference compared with the control group. Plasma concentrations of neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C increased (5.6±1.3) and (7.4±1.5) times in the OA group compared to baseline values, and were significantly higher than the values in the control group. OA injection in combination with conventional MV strategy resulted in a dramatic aggravation of hemodynamic and blood gas exchange parameters, while these parameters remained stable during the experiment in the control group. The plasma expression of TNF-α and IL-6 in the OA group were significantly higher than that in the control group. Compared with high expression in the lung and renal tissue in the OA group, TNF-α and IL-6 were too low to be detected in the lung and renal tissue in the control group.
Conclusions OA injection in combination with conventional MV strategy not only resulted in a severe lung injury but also an apparent renal injury. The potential mechanisms involved a cytokine response of TNF-α and IL-6 in plasma, lung and renal tissues.
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5.
With regard to pulmonary tissue damage secondary to extracorporeal circulation, most studies focused on the pulmonary histological changes after artificial lung bypass, but none compared the pre- and post-operative pulmonary changes of artificial lung with those of autogenous lung. We compared the changes in autogenous lung oxygenation and artificial lung oxygenation during cardiopulmonary bypass (CPB). The results showed that autogenous lung oxygenation is less injurious to the lung than bubble oxygenation and is more physiological. We think that during open heart surgery with autogenous lung bypass, the lung is functioning physiologically and supplied with normal amount of oxygen, while using bubble oxygenation for CPB, the native lung, the only nonperfused organ, is insulted by pulmonary ischemia, which is one of the most important reasons for pulmonary injury after CPB.
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6.
Background With the widespread use of ventilators in treating critically ill patients, the morbidity of ventilator-induced lung injury (VILI) is increasing accordingly. VILI is characterized by a considerable increase in microvascular leakiness and activation of inflammatory processes. In this study we investigated the effects of inflammatory mediators in VILI rat serum on endothelial cytoskeleton and monolayer cellular permeability, as well as the therapeutic effect of ulinastatin, to explore the pathogenesis and the relationship between biotrauma and lung oedema induced by VILI. Methods Thirty healthy male Sprague-Dawley rats were randomly divided into three groups: group A (normal tidal volume ventilation), group B (high tidal volume ventilation) and group C (high tidal volume ventilation plus ulinastatin). The serum of each rat after ventilation was added to endothelial cell line ECV-304 medium for two hours to observe the effects of serum and/or ulinastatin on endothelial fibrous actin and permeability. Results Compared to rats ventilated with normal tidal volume, serum of rats ventilated with high tidal volume caused a striking reorganization of actin cytoskeleton with a weakening of fluorescent intensity at the peripheral filament bands and formation of the long and thick stress fibres in the centre resulting in endothelial contraction and higher permeability. Prior treatment with ulinastatin lessened the above changes significantly. The changes of permeability coefficient of endothelial permeability after group A, B or C rats serum stimulation were (6.95±1.66)%, (27.50±7.77)% and (17.71±4.66)% respectively with statistically significant differences (P<0.05) among the three groups. Conclusions The proinflammatory mediators in the serum of the rats given high tidal volume ventilation increases endothelial permeability by reorganizing actin cytoskeleton, and pretreatment with ulinastatin lessens the permeability by inhibiting of proinflammatory mediators.  相似文献   

7.
Neutrophils play a critical role in ventilation-induced lung injury. This study was aimed to investigate the characteristics of neutrophils influx in lungs induced by high tidal volume ventilation. Anaesthetized rats were randomly divided into low tidal volume ventilation group (Vt: 7 mL/kg, LV group) or high tidal volume ventilation group (Vt:42mL/kg, HV group ) (n=40 in each). Rats in each group were ventilated for 0, 60, 90, 120 and 240 min. The wet/dry lung weight ratio (W/D) was measured. The levels of macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-α (TNF-α), and the activity of myeloperoxidase (MPO) were detected by enzyme-linked immunosorbent assay (ELISA). The number of neutrophils in bronchoalveolar lavage fluid (BALF) was counted after Wright’s staining, and the percentage of netrophils in lung tissues calculated. Histopatholgical examination was used to observe the changes of lung tissues after different ventilations. The results showed that the W/D weight ratio was increased, and the levels of MIP-2 and TNF-α significantly enhanced in HV group at 90, 120 and 240 min. Neutrophils in BALF and the neutrophil percentage in lung tissues were also elevated at 120 and 240 min, which coincided with the enhanced activity of MPO in HV group. The lung injury was significantly related with the ventilation time and the infiltration of neutrophils in lungs in HV group. In conclusion, in ventilation-induced lung injury, neutrophil infiltration is present in a time-dependent manner and associated with the aggravated lung injury. Pulmonary structural damage may be the main reason for ventilation-induced lung injury.  相似文献   

8.
Objective:To study the effect and mechanism of sodium ferulate (SF) in preventing and treating ozone (O_3) induced lung oxidative injury in mice.Methods:Lung oxidative injury model mice were established by making them inhale O_3.The activity of anti-oxidase and membranous microviscosity in epithelial cells in the lung of mice were determined,and the ultrastructural change of lung tissues was observed with electromicroscopy.Results:Activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were reduced,while membranous lipo-microviscosity significantly increased in the pulmonary epithelial cells of model mice,revealing ultrastructural change.These abnormal changes were reversed by SF treatment,which was manifested as the significantly raised activities of SOD and GSH-Px after treatment with high and moderate doses of SF,showing a significant difference compared with those in the model group (P<0.01).Membranous lipo-microviscosity basically approached that in the control group (P>0.05);electron microscopic examination showed a basically normal morphological structure of pulmonary epithelial cells,with the change in lung injury significantly milder than that in the model group.Conclusion:O_3 could induce oxidative injury of lungs in mice,and SF could enhance the anti-oxidation capacity of mice and scavenge the oxygen free radicals so as to alleviate the injury.  相似文献   

9.
Mechanical ventilation, a crucial therapy to acute respiratory distress syndrome (ARDS),could exacerbate lung injury, and even result in ventilator-induced lung injury (VILI) if misused in some condition1. Over-activating inflammatory cells and expanding inflammatory responses, which are induced by infection, are fundamental reasons for ARDS. Among them,  相似文献   

10.
Background Pediatric patients are susceptible to lung injury that does not respond to traditional therapies.Partial liquid ventilation (PLV) has been developed as an alternative ventilatory strategy for treating severe lung injury.The aim of this study is to investigate the effect of PLV on lung function in immature piglets.Methods Acute lung injury was induced in 12 Chinese immature piglets by oleic acid (OA).The animals were randomly assigned to two groups (n=6 each group):(1) conventional mechanical ventilation (MV) group and (2) PLV with FC-77 (10 ml/kg) group.Mean arterial blood pressure (MAP),mean pulmonary arterial pressure (MPAP),central venous pressure (CVP),left atrial pressure (LAP),systemic vascular resistance (SVR),pulmonary vascular resistance (PVR),cardiac output (CO),mean pressure of airway (Paw),dynamic lung compliance (Cydn),and arterial blood gases were measured during the observation period.Results No piglet died in either group with severe lung injury.After four hours of ventilation,pH in the MV group gradually decreased to lower than 7.20,while in the PLV group,pH also gradually decreased but remained higher than 7.20 (P <0.05).Partial pressure of oxygen in artery (PaO2) decreased in both groups,but with a significant difference between the PLV group and MV group (P <0.05).Partial pressure of carbon dioxide in artery (PaCO2) increased in both groups,but with a significant difference between the PLV group and MV group (P <0.05).Paw increased in both groups,but was not significantly different (P >0.05).Cydn decreased in both groups,but without a significant difference (P >0.05).At four hours,heart rate (HR) and MAP in both groups decreased.MPAP in both groups increased,and there was a significant difference between the two groups (P <0.05).CVP was stable in both groups.At four hours,PVR and LAP were increased in both groups.CO was decreased in both groups (P <0.05).SVR was stable during the observation time.Conclusion PLV did not improve outcome in changes of lung function.  相似文献   

11.
Background:Subsequent neutrophil (polymorphonuclear neutrophil [PMN])-predominant inflammatory response is a predominant feature of ventilator-induced lung injury (VILI),and mesenchymal stem cell (MSC)...  相似文献   

12.
目的 通过观察AngⅡ受体拮抗剂——氯沙坦对呼吸机所致肺组织TNF-α水平和髓过氧化物酶(MPO)活性的影响,探讨氯沙坦对呼吸机所致肺损伤的保护作用.方法 24只健康雄性Wister大鼠随机分为对照组、呼吸机所致肺损伤组(VILI)和氯沙坦干预组(LAP),分别采用ELISA法测定大鼠肺组织中血管紧张素Ⅱ( AngⅡ)含量,采用免疫组织化学染色法测定大鼠肺组织TNF-α蛋白表达水平,采用化学比色法测定肺组织匀浆中MPO活性.结果 VILI组大鼠肺组织AngⅡ含量、TNF-α蛋白表达水平以及肺组织匀浆中MPO活性均明显高于对照组(均P<0.01).氯沙坦干预组大鼠肺组织AngⅡ含量与VILI组比较无明显差异(P>0.05),但肺组织TNF-α蛋白表达水平、肺组织匀浆中MPO活性和肺W/D比值均较VILI组明显降低(均P<0.01),同时肺组织病理损伤程度也较VILI组明显减轻.结论 AngⅡ通过调控肺组织中TNF-α的表达在VILI发病中起重要作用,氯沙坦可阻断AngⅡ与AT1受体的结合,下调肺组织TNF-α表达,降低MPO的活性,对VILI具有一定防治作用.  相似文献   

13.
[摘要] 目的 探讨丙泊酚对呼吸机所致肺损伤大鼠肺部促分裂原活化蛋白激酶和炎症反应的影响。方法 SD大鼠随机均分成3组:常规潮气量通气组(C组),大潮气量通气组(H组)和丙泊酚处理组(P组)。P组在通气同时给予丙泊酚,C组和H组给予生理盐水。收集肺灌洗液和组织标本,测量肺组织湿/干比,观察肺病理改变,检测支气管肺泡灌洗液中总蛋白、白介素1β和白介素6的含量,Western Blot方法检测各组肺组织中促分裂原活化蛋白激酶及其和磷酸化水平。结果 C组大鼠肺部未见明显的病理改变,H组和P组肺部有明显的病理改变,而P组大鼠肺部病理改变较H组明显减轻;H组和P组肺组织湿/干比、p-p38,BALF中白细胞总数、总蛋白含量、IL-1β和IL-6水平明显高于C组,上述指标P组明显低于H组。结论 丙泊酚能够减轻大潮气量机械通气造成的大鼠肺损伤,其机制可能部分与阻断促分裂原活化蛋白激酶活化以及肺部炎症有关。  相似文献   

14.
血红素氧合酶1干预对呼吸机所致肺损伤的影响   总被引:1,自引:0,他引:1  
目的探讨血红素氧合酶1(HO-1)的干预对家兔呼吸机所致肺损伤(VILI)的影响。方法 24只家兔随机分为常规潮气量+PEEP组(C组)、呼吸机所致肺损伤组(VILI组)、呼吸机所致肺损伤+HO-1诱导剂干预组(Hm组);实验终点行动脉血气分析,Western blot和免疫组化方法检测肺组织HO-1的表达水平和细胞定位,观察肺组织形态变化并进行肺损伤评分,测定肺组织湿干重比值。结果 VILI组较C组HO-1蛋白表达水平升高,HO-1蛋白主要定位于肺泡上皮细胞和血管内皮细胞,在肺泡巨噬细胞和中性粒细胞也有表达。Hm组与VILI组比较,HO-1蛋白表达水平升高,PaO2/FiO2升高,肺湿干重比值和肺损伤评分降低,差异有统计学意义(P〈0.05)。结论 HO-1蛋白表达升高能减轻VILI,对VILI有一定的保护作用。  相似文献   

15.
黄涛  ;高巨  ;徐军美 《医学综述》2014,(12):2173-2175
机械通气在危重病患者的救治过程中起着非常重要的作用,然而使用不当,可以诱发或者加重肺损伤,即呼吸机相关性肺损伤(VILI)。随着对VILI发病机制的不断探索,并采取了一些相应的防治措施,例如保护性通气模式、生物防治等,能在一定程度上减轻VILI的损伤程度。该文就机械通气肺损伤的发生机制、防治策略等方面的研究新进展予以综述。  相似文献   

16.
丁宁  肖慧  许立新  佘守章 《医学争鸣》2009,(21):2345-2347
目的:筛选呼吸机所致肺损伤(VILI)高迁移率族蛋白B1(HMGB1)的启动子结合蛋白.方法:制备VILI大鼠模型,与正常对照组大鼠同期处死,取肺组织提取细胞核蛋白.用PCR法扩增末端带生物素标记的HMGB1启动子探针,将细胞核蛋白与制备的HMGB1启动子探针进行孵育,再以标记有链亲和素的磁珠分离HMGB1启动子-蛋白反应复合物,分别用0.25mol/L和1mol/LNaCl洗脱探针上结合的蛋白,SDS-PAGE电泳分离样品蛋白,并对凝胶进行银染显色,比较VILI组与正常对照组的差异条带.结果:两组细胞核蛋白中共观察到24条差异条带.分析差异条带显示,与正常对照组比较,在低亲和力作用水平,机械通气后有6个蛋白与HMGB1启动子的结合力增强,有2个蛋白的结合力减弱;在高亲和力作用水平,有10个蛋白与HMGB1启动子的结合力增强,有6个蛋白的结合力减弱.结论:筛选到一些VILI特异性HMGB1启动子结合蛋白,对于研究HMGB1的转录调控机制具有重要意义.  相似文献   

17.
目的 探讨沙丁胺醇对老年大鼠呼吸机相关肺损伤(VILI)的干预作用.方法 将24只雄性Wistar老龄大鼠随机分为3组:正常对照组(第1组)、VILI未治疗组(第2组)、沙丁胺醇治疗组(第3组),各接受不同潮气量的通气,通气时间为4h.检测各组大鼠左肺肺组织黄嘌呤氧化酶(XOD)与超氧物歧化酶(SOD)的活性,以及IL-2、IL-6、IL-8、TNF-α和丙二醛(MDA)的含量,同时观察肺组织HE染色和电镜下的变化.结果 第2组大鼠肺组织SOD与XOD的活性较第1组显著降低,而第3组较第2组明显提高(P均<0.01).第2组大鼠肺组织MDA、TNF-α、IL-2和IL-6含量较第1组升高(P均<0.01),第3组较第2组则显著降低(P均<0.01),各组大鼠肺组织IL-8含量差异无统计学意义(P>0.05);第2组大鼠肺组织HE染色显示炎症浸润明显,第3组较第2组明显减轻;电镜下第2组大鼠肺组织细胞及细胞器肿胀,毛细血管大量开放、充血,中性粒细胞激活,肺泡透明膜形成,第3组以上表现较第2组明显减轻.结论 沙丁胺醇能够减轻老年大鼠呼吸机相关肺损伤的炎症反应,提高了多种抗氧化物质的活性,改善微循环,从而减轻肺水肿的程度,对肺组织起到一定的保护作用.  相似文献   

18.
目的以大鼠呼吸机相关性肺损伤(VILI)为模型,用血晶素(hemin)诱导大鼠血红素加氧酶-1(HO-1)表达,观察VILI时超氧化物歧化酶(SOD)和丙二醛(MDA)活性变化及HO-1对SOD和MDA的影响,探讨在VILI过程中的抗氧化应激保护作用及其机制。方法32只雄性SD大鼠随机分成4组(每组n=8):对照组只做气管切开术,保留自主呼吸;模型组气管切开后行机械通气4 h;诱导剂组于模型制备前24 h腹腔注射血晶素40μmol/kg;抑制剂组于模型制备前24 h腹腔注射锌原卟啉(ZnPP)10μmol/kg。机械通气4 h后处死大鼠,收集肺组织和支气管肺泡灌洗液(BALF)标本,测定BALF中总蛋白含量,肺组织湿/干重比值(W/D),肺组织LDH、SOD活性和MDA含量,检测肺组织HO-1蛋白表达,光镜下行肺组织病理学观察。结果与对照组相比,模型组大鼠肺组织病理损伤严重,肺W/D、BALF中总蛋白、LDH活性均明显增加,VILI模型复制成功。与模型组比较,诱导剂组肺组织HO-1表达增加,肺组织病理损伤明显减轻,SOD活性明显增加而MDA含量明显下降,用ZnPP抑制HO-1表达,此种保护作用消失。结论血晶素诱导大鼠HO-1表达可以增加SOD活性,降低MDA含量,减轻肺的氧化应激损伤,降低VILI的程度。  相似文献   

19.
目的 探讨通气相关肺损伤(ventilator induced lung injury,VILI)中的肺部炎症反应和肺内血管紧张素Ⅱ的关系,并研究血管紧张素转换酶抑制剂(卡托普利)在大鼠通气相关肺损伤模型中的作用.方法 将21只雄性SD大鼠分成3组:高潮气量、零呼气末正压(HVZP)组;卡托普利治疗组(HVZP+CAP)gi;空白对照组.行动脉插管和气管插管后测定动脉血气分析和平均动脉压,同时测定支气管肺泡灌洗液中的总蛋白数、巨噬细胞炎性蛋白-2(MIP-2)的浓度及肺组织血管紧张素Ⅱ的水平,并观察肺组织形态学的变化.结果 HVZP+CAP组大鼠的平均动脉压明显低于HVZP组(P<0.05).HVZP大鼠肺泡灌洗液中的总蛋白水平明显高于对照组(P<0.05),且灌洗液中的MIP-2和肺血管紧张素Ⅱ明显高于对照组和HVZP+CAP组(P<0.05).肺血管紧张素Ⅱ的水平与肺泡灌洗液中的蛋白水平和MIP-2的水平呈正相关.结论 卡托普利通过下调炎症因子可以降低机械通气中肺损伤的程度,机械通气相关肺损伤的发生与肺部的血管紧张素系统相关.  相似文献   

20.
涂惠英 《医学综述》2011,17(4):489-491
呼吸机相关性肺损伤(Ventilator-associated lung injury,VILI)是机械通气引起的严重并发症,目前临床上仍然缺乏完全有效的治疗策略。随着对VILI发病机制的不断深入研究,Toll样受体依赖的信号转导通路被认为参与了VILI的发生发展。Toll样受体识别相关配体后,通过启动细胞内外信号级联反应,介导肺部炎性因子的释放及释放后的病理生理改变。深入研究Toll样受体在VILI中的作用,可为临床提供参考。  相似文献   

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