Effect of captopril on apoptosis induced by high tidal volume ventilation in lung tissue of rats
Mingxia Hou, Xinri Zhang
Abstract
Mingxia Hou, Xinri Zhang
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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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
Key concepts: Captopril, Medicine, Lung, Apoptosis, TUNEL assay, Tidal volume, Ventilation (architecture), Internal medicine