驱动压对肺内源性急性呼吸窘迫综合征的影响

目的探讨不同驱动压力对脂多糖诱导的肺内源性急性呼吸窘迫综合征（ARDS）的治疗作用及其机制。 方法40只雄性Sprague-Dawley大鼠分为对照组、急性呼吸窘迫综合征模型组（ARDS组）、机械通气低驱动压组（L组）、机械通气一般驱动压组（M组）、机械通气高驱动压组（H组），每组各8只。气管内滴注脂多糖6 mg/kg复制ARDS动物模型，模型复制成功后对L组、M组及H组实施相应的机械通气策略4 h。比较5组大鼠动脉血氧分压（PaO₂）、二氧化碳分压（PaCO₂）、肺组织湿/干重比、肺泡灌洗液（BALF）中总蛋白、Ⅲ型前胶原（PCⅢ）、血清中白细胞介素6（IL-6）的表达水平以及肺组织病理形态学变化情况。 结果5组大鼠PaO₂、PaCO₂、肺组织湿/干重比、BALF中蛋白含量、血清IL-6、PCⅢ表达水平、塌陷肺泡所占比例以及膨胀肺泡所占比例比较，差异均有统计学意义（F= 25.054、5.316、14.306、84.940、93.379、41.983、49.343、123.433，P均< 0.05）。进一步两两比较发现，L组和H组PaO₂、肺组织湿/干重比、BALF中蛋白含量、血清IL-6以及塌陷肺泡所占比例与ARDS组比较，差异均有统计学意义（P均< 0.05），H组PaCO₂表达水平和膨胀肺泡所占比例与ARDS组比较，差异均有统计学意义（P均< 0.05），L组PCIⅢ表达水平较ARDS组显著降低（P < 0.05）；H组PaO₂、血清IL-6、PCⅢ表达水平、塌陷肺泡所占比例以及膨胀肺泡所占比例与ARDS组比较，差异均有统计学意义（P均< 0.05）。 结论在小潮气量通气下，较低的驱动压力能够改善脂多糖诱导的肺内源性ARDS大鼠的气体交换，减轻肺水肿，降低炎症反应；当驱动压过高时可能引起肺过度膨胀，甚至诱发肺损伤的发生。

Effect of driving pressure on pulmonary endogenous acute respiratory distress syndrome

ObjectiveTo investigate the effect of different driving pressure on pulmonary endogenous acute respiratory distress syndrome (ARDS) induced by lipopolysaccharide and its mechanism. MethodsForty male Sprague-Dawley rats were divided into the control group, ARDS group, mechanical ventilation low driving pressure group (L group), mechanical ventilation medium driving pressure group (M group), and mechanical ventilation high driving pressure group (H group), 8 rats in each group. The ARDS model was established by intratracheal instillation of lipopolysaccharide (6 mg/kg). Then the corresponding mechanical ventilation strategies were applied to L, M and H groups for 4 h. The expressions of arterial partial pressure of oxygen (PaO₂), partial pressure of carbon dioxide (PaCO₂), wet/dry weight ratio of lung tissue (W/D), total protein in bronchoalveolar lavage fluid (BALF), type Ⅲ procollagen (PCⅢ) and interleukin 6 (IL-6) in serum, and the pathological and morphological changes of lung tissue were compared in these five groups. ResultsThere were significant differences in the expressions of PaO₂, PaCO₂, wet/dry weight ratio of lung tissu, protein content in BALF, IL-6 in serum and PCⅢ, and the proportion of collapsed alveoli and inflated alveoli in these five groups (F= 25.054, 5.316, 14.306, 84.940, 93.379, 41.983, 49.343, 123.433; all P < 0.05). Further comparison showed that the expressions of PaO₂, W/D of lung tissue, protein content in BALF and IL-6 in serum, and the proportion of collapsed alveoli in L and H groups were significantly different compared with ARDS group (all P < 0.05). The expression of PaCO₂ and the proportion of inflated alveoli in H and ARDS groups were significantly different (both P < 0.05). The PCⅢ expression was significantly lower in the L group than in ARDS group (P < 0.05). The expressions of PaO₂, IL-6 in serum and PCⅢ, and the proportion of collapsed alveoli and inflated alveoli in H and ARDS groups were significantly different (all P < 0.05). ConclusionsUnder low tidal volume ventilation, lower driving pressure can improve gas exchange and reduce pulmonary edema and inflammatory response in lipopolysaccharide induced lung endogenous ARDS rats. High driving pressure may cause excessive lung expansion and lead to lung injury.