Effects of peak inspiratory flow on development of ventilator-induced lung injury in rabbits

BACKGROUND: A lung-protecting strategy is essential when ventilating acute lung injury/acute respiratory distress syndrome patients. Current emphasis is on limiting inspiratory pressure and volume. This study was designed to investigate the effect of peak inspiratory flow on lung injury. METHODS: Twenty-four rabbits were anesthetized, tracheostomized, ventilated with a Siemens Servo 300, and randomly assigned to three groups as follows: 1) the pressure regulated volume control group received pressure-regulated volume control mode with inspiratory time set at 20% of total cycle time, 2) the volume control with 20% inspiratory time group received volume-control mode with inspiratory time of 20% of total cycle time, and 3) the volume control with 50% inspiratory time group received volume-control mode with inspiratory time of 50% of total cycle time. Tidal volume was 30 ml/kg, respiratory rate was 20 breaths/min, and positive end-expiratory pressure was 0 cm H2O. After 6 h mechanical ventilation, the lungs were removed for histologic examination. RESULTS: When mechanical ventilation started, peak inspiratory flow was 28.8 +/- 1.4 l/min in the pressure regulated volume control group, 7.5 +/- 0.5 l/min in the volume control with 20% inspiratory time group, and 2.6 +/- 0.3 l/min in the volume control with 50% inspiratory time group. Plateau pressure did not differ significantly among the groups. Gradually during 6 h, Pao2 in the pressure regulated volume control group decreased from 688 +/- 39 to a significantly lower 304 +/- 199 mm Hg (P < 0.05) (mean +/- SD). The static compliance of the respiratory system for the pressure regulated volume control group also ended significantly lower after 6 h (P < 0.05). Wet to dry ratio for the pressure regulated volume control group was larger than for other groups (P < 0.05). Macroscopically and histologically, the lungs of the pressure regulated volume control group showed more injury than the other groups. CONCLUSION: When an injurious tidal volume is delivered, the deterioration in gas exchange and respiratory mechanics, and lung injury appear to be marked at a high peak inspiratory flow.     

金雀异黄素预先给药对大鼠机械通气所致肺损伤的作用

目的 研究特异性蛋白酪氨酸激酶抑制剂金雀异黄素预先给药对大鼠机械通气所致肺损伤（VILI）的作用。方法 30只健康SD大鼠，随机分为3组，每组10只，A组采用8ml／kg潮气量机械通气；B组采用40ml／kg潮气量机械通气；C组采用40ml／kg潮气量机械通气，并在机械通气前30min腹腔注射金雀异黄素50mg／kg。3组呼吸频率均为80次／min，吸／呼比（I：E）为1：1，PEEP为0，吸人气体为室内空气。机械通气2h后处死大鼠，取肺组织，光镜下观察病理学，测定髓过氧化物酶（MPO）活性、磷酸化p38（p-p38）、p38水平；收集支气管肺泡灌洗液，测定总蛋白、肿瘤坏死因子-α（TNF-α）水平，并进行白细胞（WBC）计数。结果与A组比较，B组支气管肺泡灌洗液总蛋白、WBC计数、TNF-α及肺组织MPO、P—p38／p38水平升高（P〈0．05或0．01），肺组织病理学改变严重；与B组比较，C组上述指标降低（P〈0．01或0．05），肺组织病理学改变明显减轻。结论 金雀异黄素50mg／kg预先给药可减轻大鼠VILI，其机制与抑制了p38通路的激活有关。     

半乳糖凝集素-1预处理对机械通气相关性肺损伤小鼠的影响

目的 探讨半乳糖凝集素-1(Galectin-1)预处理对机械通气相关性肺损伤(VILI)小鼠的影响。方法 选择清洁级健康雄性C57BL/6小鼠30只,6～8周龄,体重22～30 g。采用随机数字表法将小鼠分为三组：对照组(C组)、VILI组(V组)和Galectin-1+VILI组(G组),每组10只。C组气管插管后保持自主呼吸4 h, V组和G组气管插管后机械通气4 h。气管插管前1 h C组和V组腹腔注射生理盐水0.75 ml, G组腹腔注射Galectin-1 3μg。于气管插管前即刻、自主呼吸或机械通气结束时采集动脉血检测PaO₂,后处死小鼠,收集肺泡支气管灌洗液(BALF),采用ELISA法检测BALF中IL-1β和IL-18浓度。取肺组织测定湿/干重比(W/D),采用qRT-PCR法检测肺组织GSDMD、caspase-1和caspase-11 mRNA表达量,Western blot法检测肺组织GSDMD、caspase-1和caspase-11蛋白含量,HE染色法观察病理改变并行肺损伤评分。结果 与C组比较,V组和G组机械通气结束时PaO     

Effect of ventilator-induced lung injury on the development of reperfusion injury in a rat lung transplant model

OBJECTIVE: Although mechanical ventilation can potentially worsen preexisting lung injury, its importance in the setting of lung transplantation has not been explored. This study was undertaken to examine the effect of 2 ventilatory strategies on the development of ischemia-reperfusion injury after lung transplantation. METHODS: In a rat lung transplant model animals were randomized into 2 groups defined by the ventilatory strategy during the early reperfusion period. In conventional mechanical ventilation the transplanted lung was ventilated with a tidal volume equal to 50% of the inspiratory capacity of the left lung and a low positive end-expiratory pressure. In minimal mechanical stress ventilation the transplanted lung was ventilated with a tidal volume equal to 20% of the inspiratory capacity of the left lung, and positive end-expiratory pressure was adjusted according to the shape of the pressure-time curve to minimize pulmonary stress. RESULTS: After 3 hours of reperfusion, oxygenation from the transplanted lung was significantly higher with minimal mechanical stress ventilation than with conventional ventilation. In addition, elastance, cytokine levels, and morphologic signs of injury were significantly lower in the group with minimal mechanical stress ventilation. CONCLUSIONS: This study demonstrates that the mode of mechanical ventilation used in the early phase of reperfusion of the transplanted lung can influence ischemia-reperfusion injury, and a protective ventilatory strategy on the basis of minimizing pulmonary mechanical stress can lead to improved lung function after lung transplantation.     

参附注射液对大鼠机械通气相关性肺损伤的保护作用及其机制

目的 探讨参附注射液(Shenfu injection,SF)对大鼠机械通气(mechanical ventilation,MV)相关性肺损伤的保护作用及其机制. 方法 40只健康成年雄性Wister大鼠采用随机数字表法分为4组,每组10只:对照组(C组)、正常潮气量MV组(N组)、大潮气量MV组(L组)、大潮气量MV+SF处理组(SF组).C组保留自主呼吸;N组、L组和SF组MV4h,潮气量分别设置为8～10 ml/kg、40 ml/kg、40 ml/kg,SF组于MV前15 min静脉注射SF 10 ml/kg.实验结束处死动物,收集支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF),测定BALF中总蛋白、IL-1β、IL-18和TNF-α的浓度;取肺组织,测量湿/干重比(wet/dry,W/D),采用免疫组化法检测肺组织NF-κB的表达,观察病理学改变并进行肺损伤评分. 结果 SF组BALF中TNF-α、IL-1β、IL-18浓度分别为(65±11)、(47±9)、(58±8) ng/L,较L组(99±7)、(69±7)、(86±7) ng/L明显降低(P＜0.05);SF组大鼠肺损伤评分、W/D、肺组织NF-κB光密度值分别为(8.5±1.8)分、(5.0±1.6)、(0.32±0.28),较L组(14.1±2.7)分、(5.5±1.8)、(0.54±0.33)均明显降低(P＜0.05). 结论 SF可减轻大鼠MV相关性肺损伤,其机制可能与SF抑制肺内NF-κB通路的活性且降低肺内炎性因子的释放有关.     

不同剂量瘦素对大鼠机械通气肺损伤的影响

目的评价不同剂量瘦素对大鼠机械通气肺损伤的影响。方法健康清洁级SD雄性大鼠48只,6～8周龄,采用随机数字表法分为四组:气管切开保留自主呼吸的假手术组(A组)、机械通气模型组(B组)、瘦素10μg/kg组(C组)和瘦素50μg/kg组(D组),每组12只。采用10%水合氯醛3.5 ml/kg麻醉大鼠,疼痛反射消失后C组腹腔注射瘦素10μg/kg,D组腹腔注射瘦素50μg/kg,A、B组腹腔注射等容量生理盐水,注射后即刻进行气管切开,插管机械通气。A组气管插管后保留自主呼吸,B、C、D组机械通气建立VILI模型,参数设置:V_T 20 ml/kg,RR 80次/分,I∶E 1∶1,FiO_2 21%,PEEP 0 mmHg,通气时间4 h。分别于基础状态、通气结束时抽取股动脉血进行血气分析。通气结束后放血处死大鼠,在4℃下取肺组织并收集支气管肺泡灌洗液(bronchoalveolar lavage fluid, BALF),光镜下进行中性粒细胞计数,采用ELISA法测定TNF-α、IL-6、IL-1β浓度;取肺组织称重,计算肺湿干重比(W/D);观察肺组织病理改变并进行病理评分;采用Western blot检测肺组织研磨液中NF-κB p65含量。结果与A组比较,B、C、D组W/D、肺损伤评分、BALF中性粒细胞计数、TNF-α、IL-6、IL-1β浓度及肺组织NF-κB p65含量明显升高(P0.01)。与B组比较,C、D组BALF中性粒细胞计数、TNF-α、IL-6、IL-1β浓度及肺组织肺损伤评分、NF-κB p65含量明显降低(P0.05)。与C组比较,D组BALF中性粒细胞计数、TNF-α、IL-6、IL-1β浓度及肺组织肺损伤评分、NF-κB p65含量明显降低(P0.05)。结论瘦素可降低大鼠机械通气肺损伤中炎性因子的表达水平,减轻肺损伤,50μg/kg较10μg/kg作用明显。     

氟比洛芬酯对大鼠机械通气所致肺损伤的影响

目的 探讨氟比洛芬酯对大鼠机械通气所致肺损伤的影响.方法 健康成年雄性SD大鼠40只,体重300～350 g,随机分为4组(n=10),常规潮气量通气组(TV组,潮气量8 ml/ks)、大潮气量通气组(HV组,潮气量40 ml/ks)、大潮气量通气+氟比洛芬酯5 ms/kg组(HV+F1组)和大潮气量通气+氟比洛芬酯10 mg/kg组(HV+F2组).HV+F1组和HV+F2组于机械通气前15 min时分别静脉注射氟比洛芬酯5、10 mg/ks.于机械通气4 h时处死大鼠,测定支气管肺泡灌洗液(BALF)肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、血栓素B2(TXB2)和总蛋白浓度,计数白细胞及计算肺组织湿/干重比(W/D),光镜下观察肺组织病理学结果.结果 与TV组相比,HV组BALF TNF-α、IL-6、TXB2、总蛋白浓度、白细胞计数和肺组织W/D升高(P<0.05),肺组织发生病理学损伤;与HV组相比,HV+F1组和HV+F2组BALF TNF-α、IL-6、TXB2、总蛋白浓度、白细胞计数和肺组织W/D降低(P<0.05),肺组织病理学损伤减轻;HV+F2组BALF TNF-α和TXB2浓度低于HV+F1组(P<0.05),其余指标差异均无统计学意义(P>0.05).结论 氟比洛芬酯可通过抑制炎性反应减轻大鼠机械通气所致肺损伤.     

Effect of inspiratory flow rate on bronchomotor tone in normal and asthmatic subjects

The effect of the inspiratory flow rate during deep inspiration on the regulation of bronchomotor tone was studied in nine normal and 22 asthmatic subjects. Changes in bronchial tone were assessed by respiratory resistance measured by an oscillation method. In normal subjects with bronchoconstriction induced by methacholine a rapid deep inspiration reduced respiratory resistance more than a slow deep inspiration. Asthmatic subjects with spontaneous airway narrowing showed an increase in respiratory resistance after deep inspiration that was greater after rapid than after slow deep inspiration. On the other hand, in asthmatics with methacholine induced bronchoconstriction, bronchodilatation occurred after deep inspiration and this was also greater after rapid than after slow deep inspiration. Lignocaine inhalation attenuated both bronchoconstriction and bronchodilatation induced by both slow and rapid deep inspiration. These results suggest that the effects of deep inspiration are mediated at least in part via receptors in the airways. It is suggested that in asthmatic patients with spontaneous bronchoconstriction irritant receptor activity will be increased in proportion to the speed of inspiration. After methacholine induced bronchoconstriction stretch receptor activity is likely to behave in a similar fashion, leading to an opposite effect.     

异丙酚减轻大鼠机械通气所致肺损伤

目的探讨异丙酚对大鼠高压力机械通气所致急性肺损伤的影响。方法24只Wistar大鼠随机分为3组（n=8）,采用压力控制机械通气模式通气。A组为对照组,通气模式为PIP=25 cmH2O,PEEP=2 cm H2O;B、C两组为异丙酚组,通气模式同A组,B组输注模式为静注2 mg／kg,继以4 mg·ks^-1·h^-1速度持续输注;C组输注模式为静注5 mg／kg,继以10 mg·kg^-1·h^-1速度持续输注,记录基础时点、1h、2 h、3 h、4 h的MAP、HR和动脉血气。4 h后处死全部大鼠。测量肺组织湿干比、BALF中蛋白含量,观察肺组织病理形态学变化。结果A组MAP、PaO2和pH在4 h时显著降低,与基础值相比有统计学差异（P〈 0．05）,而B、C两组与基础值相比无明显变化。在4h时A组的PaCO2显著升高（P〈0．05）,而B、C两组与基础值相比无明显变化。肺组织湿／干比和BALF中蛋白含量A组亦明显高于B、C两组（P〈0．05）。B、C组间无显著差别。肺组织形态学改变B、C组好于A组,肺组织中性粒细胞浸润程度也较轻。结论异丙酚对机械通气所致急性肺损伤具有保护作用,其机制可能与减少中性粒细胞在肺内浸润有关。     

七氟醚减轻大鼠呼吸机相关性肺损伤

目的 探讨七氟醚对大鼠呼吸机相关性肺损伤(VILI)的影响并探讨其可能机制。方法 健康SPF级雄性SD大鼠36只,6～8周龄,体重220～280 g。随机分为三组：对照组(C组)、VILI组(V组)和七氟醚组(S组),每组12只。大鼠给予1%戊巴比妥钠40 mg/kg麻醉后行气管切开插管术,C组自主呼吸4 h, V组和S组插管后机械通气4 h, S组机械通气期间吸入2%七氟醚4 h。通气参数：V_T 20 ml/kg, RR 80次/分,I∶E 1∶1,FiO₂ 21%,PEEP 0 cmH₂O。机械通气结束时采集股动脉血测定PaO₂。处死大鼠,取肺组织和支气管肺泡灌洗液(BALF),计算肺组织湿/干重比值(W/D),采用ELISA法检测BALF中白细胞介素(IL)-1β、IL-18浓度,二氯荧光黄双乙酸盐法检测BALF中肺泡巨噬细胞活性氧(ROS)水平,Western blot法及qRT-PCR法检测肺组织NF-E2相关因子2(Nrf2)、NLRP3、凋亡相关斑点样蛋白(ASC)、caspase-1...     

Ventilation-perfusion distribution related to different inspiratory flow patterns in experimental lung injury

In acute lung injury (ALI), controlled mechanical ventilation with decelerating inspiratory flow (.V(dec)) has been suggested to improve oxygenation when compared with constant flow (.V(con)) by improving the distribution of ventilation and perfusion (.V(A)/.Q). We performed the present study to test this hypothesis in an animal model of ALI. Furthermore, the effects of combined decelerating and constant flow (Vdot;(deco)) were evaluated. Thus, 18 pigs with experimental ALI were randomized to receive mechanical ventilation with either .V(con), .V(dec) or a fixed combination of both flow wave forms (.V(deco)) at the same tidal volume and positive end-expiratory pressure level for 6 h. Hemodynamics, gas exchange, and .V(A)/.Q distribution were determined. The results revealed an improvement of oxygenation resulting from a decrease of pulmonary shunt within each group (P < 0.05). However, blood flow to lung areas with a normal .V(A)/.Q distribution increased only during ventilation with .V(con) (P < 0.05). Accordingly, PaO(2) was higher with .V(con) than with .V(dec) and .V(deco) (P < 0.05). We conclude that contrary to the hypothesis, .V(con)provides a more favorable .V(A)/.Q distribution, and hence better oxygenation, when compared with .V(dec) and .V(deco) in this model of ALI. IMPLICATIONS: In acute lung injury, mechanical ventilation with decelerating flow has been suggested to improve ventilation-perfusion distribution when compared with constant flow. We tested this hypothesis in an animal model. Contrary to the hypothesis, we found a more favorable ventilation-perfusion distribution during constant flow when compared with decelerating flow.     

From continuous positive-pressure breathing to ventilator-induced lung injury

Continuous positive-pressure ventilation in acute respiratory failure. By Kumar A, Falke KJ, Geffin B, Aldredge CF, Laver MB, Lowentein E, Pontoppidan H. N Engl J Med 1970; 283:1430-6. Reprinted with permission.Continuous positive-pressure ventilation was used in eight patients with severe acute respiratory failure. Cardiac output and lung function were studied during continuous positive-pressure ventilation (mean end-expiratory pressure, 13 cm H2O) and a 30-min interval of intermittent positive-pressure ventilation. Although the mean cardiac index increased from 3.6 to 4.5 l/min per square meter of body surface area, the mean intrapulmonary shunt increased by 9% with changeover to intermittent positive-pressure ventilation. Satisfactory oxygenation was maintained in all patients during continuous positive-pressure ventilation with 50% inspired oxygen or less. With intermittent positive-pressure ventilation, arterial oxygen tension promptly fell by 161 mm of mercury, 79% occurring within 1 min. Prevention of air-space collapse during expiration and an increase in functional residual capacity probably explain improved oxygenation with continuous positive-pressure ventilation. In four patients, subcutaneous emphysema or pneumothorax developed. Weighed against the effects of prolonged hypoxemia, these complications were not severe enough to warrant cessation of continuous positive-pressure ventilation.     

丙泊酚对大鼠机械通气相关肺损伤的保护作用及机制

Objective To investigate the mechanisms of propofol on ventilator-induced lung injury in rats produced by high PIP ventilation. Methods Twenty-four anesthetized Wistar rats weighting 280 g-320 g were randomly divided into tlhree groups (n=8). Rats were ventilated with high PIP pattern (PIP=25 cm H2O,PEEP=2 cm H2O) for 4 h. Propofol was given in a bolus of 2 mg/kg (group B) or 5 mg/kg (group C), followed by continuous infusion with 4 mg·kg-1·h-1 (group B)or 10 mg·kg-1·h-1(group C). No Propofol was given for group A. MAP, HR were recorded and arterial blood gases were analyzed. Lung wet and dry weight ratio( W/D), tumor necrosis factora(TNF-α), interleukin1β(IL-1β), IL-6, IL-10, macrophage inflammatory protein2(MIP-2) and protein content in bronchoalveolar lavage fluid (BALF) , content of malondialdehyde (MDA) and superoxide dismutase (SOD) in lung homogenate were determined.Pathological change of lung was examined and lung injury was scored as well. Results MAP and PaO2 decreased from (116±7.4) mm Hg and (379±65) mm Hg to (73±21 )mm Hg and (103±48)mm Hg, and PaCO2 increased at fourth hour in group A(P<0.05). PaO2 in group B and C were higher than in group A after 3 h(P<0.05). Lung W/D weight ratio, TNF-α, MIP-2 and protein content in BALF were higher in group A (P<0.05), and MDA was higher in group A (P<0.05). No significant difference between group B and C. Pathological changes of lung in group B and C were all better than those in group A. Conclusion Propofol may attenuate VILI in rats partly by reducing the release of cytokine, decreasing the accumulation of neutrophil in the lung, and inhibiting peroxidized injury.     

桑菊清解汤对大鼠呼吸机相关性肺损伤的影响

目的 评价桑菊清解汤对大鼠呼吸机相关性肺损伤的影响.方法 健康成年SD大鼠36只,雌雄不拘,体重300～ 350 g,采用随机数字表法,将其随机分为3组(n=12):对照组(C组)、机械通气组(V组)和桑菊清解汤组(SJ组).采用大潮气量(VT=40 ml/kg)机械通气2.5h制备大鼠呼吸机相关性肺损伤模型.SJ组于术前10 d采用桑菊清解汤300 g灌胃,1次/d,于第10次灌胃后2h时开始制备模型,V组和C组给予等容量生理盐水.于机械通气前(T0)、机械通气结束(T1)、机械通气后30 min(T2)时采集股动脉血样测定动脉血气,计算呼吸指数(RI)和氧合指数(OI),然后处死大鼠,取肺组织,采用双抗体夹心ELISA法测定肺组织TNF-α、IL-6和IL-10的含量,测定肺组织湿/干重(W/D)比,光镜下观察肺组织病理学结果.结果 与C组比较,V组和SJ组T1.2时RI升高,OI降低,肺组织TNF-α、IL-6、IL-10含量和W/D比升高(P＜0.05);与V组比较,SJ组RI降低,OI升高(P＜0.05),SJ组肺组织TNF-α、IL-6含量和W/D比降低,IL-10含量升高(P＜0.05).SJ组肺组织病理学损伤较V组减轻.结论 桑菊清解汤可减轻呼吸机相关性肺损伤,其机制与抑制炎性反应有关.     

Prevention of ventilator-induced lung injury with partial liquid ventilation

BACKGROUND/PURPOSE: Pulmonary injury from mechanical ventilation has been attributed to application of excess alveolar pressure (barotrauma) or volume (volutrauma). The authors questioned whether partial liquid ventilation (gas ventilation of the perfluorocarbon filled lung, PLV) would reduce ventilator-induced lung injury. METHODS: A tracheostomy tube and carotid artery catheter were placed in anesthetized Sprague-Dawley rats (500 +/- 50 g). Bovine serum albumin (BSA) labeled with Iodine (I) 125 was administered intraarterially. Ventilation with tidal volume (TV) of 5 mL/kg was initiated. The rats were then selected randomly to a 30-minute experimental period of one of the following ventilation protocols: continued atraumatic gas ventilation (GV, TV, 5 mL/kg; n = 10); atraumatic gas ventilation combined with intratracheal administration of 10 mL/kg perfluorocarbon (GV-PLV, TV, 5 mL/kg, n = 10); barotrauma (BT, peak inspiratory pressure [PIP], 45 cm H(2)O; n = 10); barotrauma with PLV (BT-PLV, PIP, 45 cm H(2)O; n = 8); volutrauma (VT, TV, 30 mL/kg; n = 8); or volutrauma with PLV (VT-PLV, TV, 30 mL/kg; n = 10). Animals were killed and the amount of radiolabeled BSA in both lungs was measured and normalized to the counts in 1 mL of blood from that animal (injury index). Data were analyzed by analysis of variance (ANOVA) with post-hoc t test comparison between groups. RESULTS: There was a significant difference in the (125)I-BSA injury index when all groups were compared (P <.001 by ANOVA). Post-hoc analysis showed a significant decrease in the injury index when comparing BT versus BT-PLV (P =.024) and VT versus VT-PLV (P =.014). CONCLUSION: (125)I-BSA leak produced during high-pressure or high-volume mechanical ventilation is reduced by partial liquid ventilation.     

丙泊酚对大鼠机械通气相关肺损伤的保护作用及机制

Objective To investigate the mechanisms of propofol on ventilator-induced lung injury in rats produced by high PIP ventilation. Methods Twenty-four anesthetized Wistar rats weighting 280 g-320 g were randomly divided into tlhree groups (n=8). Rats were ventilated with high PIP pattern (PIP=25 cm H2O,PEEP=2 cm H2O) for 4 h. Propofol was given in a bolus of 2 mg/kg (group B) or 5 mg/kg (group C), followed by continuous infusion with 4 mg·kg-1·h-1 (group B)or 10 mg·kg-1·h-1(group C). No Propofol was given for group A. MAP, HR were recorded and arterial blood gases were analyzed. Lung wet and dry weight ratio( W/D), tumor necrosis factora(TNF-α), interleukin1β(IL-1β), IL-6, IL-10, macrophage inflammatory protein2(MIP-2) and protein content in bronchoalveolar lavage fluid (BALF) , content of malondialdehyde (MDA) and superoxide dismutase (SOD) in lung homogenate were determined.Pathological change of lung was examined and lung injury was scored as well. Results MAP and PaO2 decreased from (116±7.4) mm Hg and (379±65) mm Hg to (73±21 )mm Hg and (103±48)mm Hg, and PaCO2 increased at fourth hour in group A(P<0.05). PaO2 in group B and C were higher than in group A after 3 h(P<0.05). Lung W/D weight ratio, TNF-α, MIP-2 and protein content in BALF were higher in group A (P<0.05), and MDA was higher in group A (P<0.05). No significant difference between group B and C. Pathological changes of lung in group B and C were all better than those in group A. Conclusion Propofol may attenuate VILI in rats partly by reducing the release of cytokine, decreasing the accumulation of neutrophil in the lung, and inhibiting peroxidized injury.