TITLE

Role of the renin-angiotensin system in ventilator-induced lung injury: an in vivo study in a rat model

AUTHOR(S)
Jih-Shuin Jerng; Yu-Chiao Hsu; Huey-Dong Wu; Hong-Zhen Pan; Hao-Chien Wang; Chia-Tung Shun; Chong-Jen Yu; Pan-Chyr Yang
PUB. DATE
June 2007
SOURCE
Thorax;Jun2007, Vol. 62 Issue 6, p527
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Injurious mechanical ventilation can cause a pro-inflammatory reaction in the lungs. Recent evidence suggests an association of the renin-angiotensin system (RAS) with lung inflammation. A study was undertaken to investigate the pathogenic role of the RAS in ventilator-induced lung injury (VILI) and to determine whether VILI can be attenuated by angiotensin converting enzyme (ACE) inhibition. Methods: Male Sprague-Dawley rats were mechanically ventilated for 4 h with low (7 mI/kg) or high (40 mI/kg) tidal volumes; non-ventilated rats were used as controls. Lung injury and inflammation were measured by the lung injury score, protein leakage, myeloperoxidase activity, pro-inflammatory cytokine levels and nuclear factor (NF)-κB activity. Expression of the RAS components was also assessed. Some rats were pretreated with the ACE inhibitor captopril (10 mg/kg) for 3 days or received a concomitant infusion with losartan or PD] 23319 (type 1 or type 2 angiotensin II receptor antagonist) during mechanical ventilation to assess possible protective effects on VILI. Results: In the high-volume group (n = 6) the lung injury score, bronchoalveolar lavage fluid protein concentration, pro-inflammatory cytokines and NF-κB activities were significantly increased compared with controls (n = 6). Lung tissue angiotensin II levels and mRNA levels of angiotensinogen and type 1 and type 2 angiotensin II receptors were also significantly increased in the high-volume group. Pretreatment with captopril or concomitant infusion with losartan or PD123319 in the high-volume group attenuated the lung injury and inflammation (n=6 for each group). Conclusions: The RAS is involved in the pathogenesis of ventilator-induced lung injury. ACE inhibitor or angiotensin receptor antagonists can attenuate VILI in this rat model.
ACCESSION #
25471943

 

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