Objective   To study the relationship between lung inflammation and lung angiotensin Ⅱ (ANGⅡ) in ventilator-induced lung injury (VILI) and assessed the efficiency of the angiotensin-converting enzyme inhibitor captopril to attenuate VILI in rats.   Methods   Totally 21 adult male Sprague-Dawley rats were randomly assigned into 3 groups

high-volume

0 positive end-expiratory pressure (HVZP) group; captopril injection (100 mg/kg i.p.) in 30 min before HVZP ventilation (HVZP+CAP group); no ventilation group (control). The blood gas tensions and mean arterial pressure were measured after a polyethylene catheter was placed in one carotid artery and a plastic cannula was inserted into the trachea. The protein contents and contents of macrophage inflammatory protein-2 (MIP-2) in bronchoalveolar lavage fluid (BALF) and lung ANGⅡ were determined by ELISA. The changes of lung pathology were observed by HE staining.   Results   Mean arterial pressure was significantly lower in the HVZP+CAP group than in the HVZP group after 2 hour’s ventilation. Total protein levels were significantly higher in BALF recovered from HVZP-ventilated rats than from controls. BALF MIP-2 and lung ANG Ⅱ were significantly higher in the HVZP group than in the control and HVZP+CAP groups. Lung ANG Ⅱ level was correlated positively with BALF contents of total protein and MIP-2.   Conclusion   Captopril has the efficiency to attenuate VILI by reducing inflammatory cytokines. Our results suggest that VILI is partly mediated by the local angiotensin system.