Effect of driving pressure on pulmonary endogenous acute respiratory distress syndrome

Abstract

Objective To investigate the effect of different driving pressure on pulmonary endogenous acute respiratory distress syndrome (ARDS) induced by lipopolysaccharide and its mechanism. Methods Forty 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. Results There 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). Conclusions Under 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. Key words: Driving pressure; Acute respiratory distress syndrome; Lipopolysaccharide