Effect Of Captopril On Apoptosis Induced By High Tidal Volume Ventilation In Lung Tissue Of Rats

ObjectiveTo explore the effect of captopril on ventilator induced lung injury(VILI) byobserving the relationship between apoptosis and angiotensin II(AngⅡ)in lungs ofrats with high tidal volume ventilation.MethodsThirty male wistar rats were randomly divided into three groups: control group，high tidal volume ventilation(H-VT) group,captopril pretreatment(CAP)group. Lungpathological changes were observed by macroscopy.The lung ALI scores、wet/dryweight ratio and the levels of protein(TP) in BALF were calculated. Apoptosis of thelung cells was detected by using terminal deoxynucleodityl transferase-mediatednick-end labeling (TUNEL). AngⅡcontents in lung tissues were detected by ELISA.Results1.The scores of acute lung injuryCompared with control group,the scores of acute lung injury were remarkablyhigher in high tidal volume ventilation group and captopril pretreatment group(P＜0.01，P＜0.05).Compared with high tidal volume ventilation group,the scores of acutelung injury were remarkably lower in captopril pretreatment group(P＜0.01).2. The ratio of wet/dry weightCompared with control group,the ratio of wet/dry weight were remarkably higherin high tidal volume ventilation group and captopril pretreatment group(P＜0.01，P＜0.05).Compared with high tidal volume ventilation group,the ratio of wet/dry weightwere remarkably lower in captopril pretreatment group(P＜0.01).3. The levels of protein in BALFCompared with control group,the levels of protein in BALF were remarkablyhigher in high tidal volume ventilation group and captopril pretreatment group(P＜0.01，P＜0.05).Compared with high tidal volume ventilation group,the levels ofprotein in BALF were remarkably lower in captopril pretreatment group(P＜0.01).4. Apoptosis index of lung cells Compared with control group, apoptosis index of lung cells were remarkablyhigher in high tidal volume ventilation group and captopril pretreatment group(P＜0.01，P＜0.05).Compared with high tidal volume ventilation group, apoptosis indexof lung cells were remarkably lower in captopril pretreatment group(P＜0.01).5. AngⅡcontents in lung tissuesCompared with high tidal volume group,angⅡcontents in lung tissues wereremarkably decreased in control group and captopril pretreatment group(all P＜0.01).There was no significant difference between control group and captoprilpretreatment group.6. Pathological changeNo substantial changes of lung morphological were observed in controlgroup.But we found that alveolar congestion,hemorrhage and infiltration oraggregation of neutrophils in airspace or vessel wall，thickness of alveolar wallmembrane formation were observed in high tidal volume group.The interstitialpulmonary edema and pneumorrhagia were significantly severer in high tidal volumegroup. Apart from captopril pretreatment group ,There was more obvious pathologicalterations in high tidal volume group.Conclusion1. Apoptosis is a crucial mechanism of VILI.2. Captopril executes lung-protective effects during mechanical ventilation viaapoptosis-suppressed with high tidal volume ventilation.