反复肺复张联合肺保护性通气对急性呼吸窘迫综合征家兔肺损伤的影响

目的 评价反复肺复张联合肺保护性通气对急性呼吸窘迫综合征(ARDS)家兔肺损伤的影响.方法 家兔24只,雌雄各半,体重2.5～3.5 kg,采用随机数字表法,将兔随机分为4组(n=6):正常对照组(Ⅰ组)、ARDS模型组(Ⅱ组)、肺保护性通气组(Ⅲ组)和反复肺复张联合肺保护性通气组(Ⅳ组).麻醉下进行机械通气,Ⅱ组、Ⅲ组和Ⅳ组采用静脉输注油酸0.1 ml/kg(经15 min输注)的方法 制备ARDS模型,模型制备成功后经3 min确定静态压力.容积曲线低位转折点.Ⅰ组和Ⅱ组的通气参数为:VT12 ml/kg,通气频率30次/min,呼气末正压(PEEP)0,FiO2 1.0,氧流量1 L/min,吸气时间0.6 s,吸呼比1.0∶2.3;Ⅲ和Ⅳ组通气参数为:VT6 ml/kg,PEEP为静态压力-容积曲线低位转折点对应气道力+2 cm H2O,其他通气参数同Ⅰ组和Ⅱ组,Ⅳ组分别在确定静态压力-容积曲线低位转折点后即刻、1、2和3 h时实施肺复张.肺复张的方法:吸气压力为30 cm H2O,吸气时间为30 s.分别于每次肺复张后采集动脉血样,测定PaO2,计算氧合指数.最后一次肺复张后1 h处死动物,取肺组织,测定TNF-α和IL-10的含量、髓过氧化物酶(MPO)活性、丙二醛(MDA)含量和湿/干重比(W/D比),计算TNF-α与IL-10的比值(TNF-α/IL-10),光镜下观察肺组织病理学结果.结果 与Ⅰ组比较,Ⅱ组氧合指数降低,肺组织TNF-α/IL-10、MPO、MDA和W/D比升高(P＜0.05);与Ⅱ组比较,Ⅲ组氧合指数升高,肺组织TNF-α/IL-10、MPO、MDA和W/D比降低(P＜0.05);与Ⅲ组比较,Ⅳ组氧合指数升高,肺组织TNF-α/IL-10、MPO、MDA和W/D比降低(P＜0.05).Ⅳ组肺组织损伤程度轻于Ⅲ组.结论 与肺保护性通气比较,肺保护性通气期间反复肺复张可进一步减轻ARDS家兔肺损伤,其机制与抑制肺组织炎性反应有关.

Abstract：

Objective To evaluate the effect of alveolar recruitment maneuvers (ARM) combined with lung protection mechanical ventilation on lung injury in a rabbit model of acute respiratory distress syndrome (ARDS) .Methods Twenty-four rabbits of both sexes weighing 2.5-3.5 kg were randomly divided into 4 groups (n=6 each):normal control group(group Ⅰ);ARDS group(group Ⅱ);ARDS+lung protection mechanical ventilation group (group Ⅲ) and ARDS + lung protection mechanical ventilation + ARM group (group Ⅳ). The animals were anesthetized with iv pentobarbital 20 mg/kg, tracheostomized and mechanically ventilated. Anesthesia was maintained with iv gammahydroxybutyrate infusion 100 mg·kg-1·h-1 and intermittent iv boluses of vecuronium. ARDS was induced with oleic acid 0.1 ml/kg injected iv over 15 min in Ⅱ ,Ⅲ and Ⅳ groups. In Ⅰand Ⅱ groups VT = 12 ml/kg, RR=30 bpm, I∶E=1.0=2.3, PEEP=0, FiO2=1, while in Ⅲ and Ⅳ groups VT=6 ml/kg, RR=30 bpm, I∶E=1.0=2.3, PEEP=airway pressure at lower inflection point+2 cm H2O, FiO2=1.ARM was performed by increasing the airway pressure to 30 cm H2O for 30 s once an hour in group Ⅳ. Arterial blood gas analysis was performed after each ARM. The animals were sacrificed at 1 h after the 3rd ARM. The lungs were removed for microscopic examination and determination of W/D lung weight ratio, TNF-α, IL-10 and MDA contents and MPO activity. TNF-α/IL-10 ratio was calculated. Results ARDS significantly decreased PaO2/FiO2 and increased TNF-α/IL-10 and W/D lung weight ratio, MPO activity and MDA content in the lung tissue. Lung protection mechanical ventilation significantly increased PaO2/FiO2 and decreased TNF-α/IL-10 and W/ D lung weight ratio, MPO activity and MDA content in the lung tissue. Lung protection mechanical ventilation + ARM significantly increased PaO2/FiO2 and decreased TNF-α/IL-10, W/D lung weight ratio, MDA content and MPO activity in group Ⅳ. Conclusion ARM combined with lung protection mechanical ventilation can further attenuate ARDS-induced lung injury by inhibiting inflammatory response.

Effect of alveolar recruitment maneuvers combined with lung protection mechanical ventilation on lung injury in a rabbit model of acute respiratory distress syndrome

Objective To evaluate the effect of alveolar recruitment maneuvers (ARM) combined with lung protection mechanical ventilation on lung injury in a rabbit model of acute respiratory distress syndrome (ARDS) .Methods Twenty-four rabbits of both sexes weighing 2.5-3.5 kg were randomly divided into 4 groups (n=6 each):normal control group(group Ⅰ);ARDS group(group Ⅱ);ARDS+lung protection mechanical ventilation group (group Ⅲ) and ARDS + lung protection mechanical ventilation + ARM group (group Ⅳ). The animals were anesthetized with iv pentobarbital 20 mg/kg, tracheostomized and mechanically ventilated. Anesthesia was maintained with iv gammahydroxybutyrate infusion 100 mg·kg-1·h-1 and intermittent iv boluses of vecuronium. ARDS was induced with oleic acid 0.1 ml/kg injected iv over 15 min in Ⅱ ,Ⅲ and Ⅳ groups. In Ⅰand Ⅱ groups VT = 12 ml/kg, RR=30 bpm, I∶E=1.0=2.3, PEEP=0, FiO2=1, while in Ⅲ and Ⅳ groups VT=6 ml/kg, RR=30 bpm, I∶E=1.0=2.3, PEEP=airway pressure at lower inflection point+2 cm H2O, FiO2=1.ARM was performed by increasing the airway pressure to 30 cm H2O for 30 s once an hour in group Ⅳ. Arterial blood gas analysis was performed after each ARM. The animals were sacrificed at 1 h after the 3rd ARM. The lungs were removed for microscopic examination and determination of W/D lung weight ratio, TNF-α, IL-10 and MDA contents and MPO activity. TNF-α/IL-10 ratio was calculated. Results ARDS significantly decreased PaO2/FiO2 and increased TNF-α/IL-10 and W/D lung weight ratio, MPO activity and MDA content in the lung tissue. Lung protection mechanical ventilation significantly increased PaO2/FiO2 and decreased TNF-α/IL-10 and W/ D lung weight ratio, MPO activity and MDA content in the lung tissue. Lung protection mechanical ventilation + ARM significantly increased PaO2/FiO2 and decreased TNF-α/IL-10, W/D lung weight ratio, MDA content and MPO activity in group Ⅳ. Conclusion ARM combined with lung protection mechanical ventilation can further attenuate ARDS-induced lung injury by inhibiting inflammatory response.