Ventilation-induced Lung Injury Increases Lung Angiotensin Ⅱ in Rats

We hypothesized that lung injury and inflammation in ventilation-induced lung injury (VILI) are related to angiotensin (Ang) Ⅱ. Adult male Sprague-Dawley rats were randomized to receive two ventilation strategies for 2 hours: 1) the high-volume zero PEEP group (HVZP) was ventilated with a high tidal volume (40mL/kg) and zero positive end expiratory pressure (PEEP); 2) the low-volume with PEEP group (LVP) was ventilated with a low tidal volume (8mL/kg) and PEEP (5cmH2O). Another group which did not receive ventilation served as the control. Total protein in bronchoalveolar lavage fluid (BALF) was significantly higher in HVZP group than in the control and LVP groups. Rats treated with HVZP ventilation had a significantly higher lung injury score than did the control and LVP groups. BALF macrophage inflammatory protein-2 (MIP-2) and lung Ang Ⅱ were significantly higher in HVZP and LVP groups when compared with the control group. Lung Ang Ⅱ correlated positively with MIP-2 in BALF in all study rats. These results indicate that local angiotensin system is involved in the pathogenesis of VILI and suggest that blockade of Ang Ⅱ might have potential therapeutic implications in alleviating VILI.