Abstract

Objective To explore the effect of captopril on ventilator induced lung injury (VILI) by observing the relationship between apoptosis and angiotensin Ⅱ (Ang Ⅱ) in lungs of rats with high tidal volume ventilation.Methods Thirty male wistar rats were randomly divided into three groups:control group,high tidal volume ventilation (H-VT) group,captopril pretreatment group.Lung pathological changes were observed by macroscopy.The lung ALI scores,wet/dry weight ratio and the levels of protein (TP) in BALF were calculated.Apoptosis of the lung cells was detected by using terminal deoxynueleodityl transferasc-mediated nick-end labeling (TUNEL).AngⅡ contents in lung tissues were detected by ELISA.Results The lung ALI scores,wet/dry weight ratio and the levels of TP in BALF,Ang Ⅱ contents and apoptotic index in H-VT group were remarkably elevated (all P<0.01),and followed by significant pathological changes of lung,Compared with H-VT group above all indexs showed marked decreased in captopril group (all P<0.01),and followed by lighter pathological changes of lung.Conclusions Apoptosis is a crucial mechanism of VILI.Captopril executes lung-protective effects during mechanical ventilation via apoptosis-suppressed with high tidal volume ventilation. Key words: Ventilator induced lung injury; Angiotensin Ⅱ; Captopril; Apoptosis

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