Angiotensin-converting enzyme inhibitor captopril attenuates ventilator-induced lung injury in rats

Objective To study the relationship between lung inflammation and lung angiotensin Ⅱ ( ANG Ⅱ) 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.