Journal
RESUSCITATION
Volume 83, Issue 7, Pages 907-912Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.resuscitation.2011.12.035
Keywords
Haemorrhagic shock; Acute lung injury; Resolution; Lipoxin; NF-kappa B
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Funding
- National Natural Science Foundation of China [30930089]
- Key Clinical Project of Ministry of Health of China [2010-47]
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Objectives: The main pathogenesis of acute lung injury induced by haemorrhagic shock is inflammation. BML-111, a lipoxinA(4)-receptor agonist, promotes acute inflammatory resolution. We sought to elucidate whether BML-111 protects haemorrhagic shock-induced acute lung injury in rats. Methods: Thirty two adult male rats were randomized to sham group (sham), haemorrhagic shock/resuscitation (HS), HS plus BML-111 (BML-111), and HS plus BML-111 and BOC-2 (BOC-2). Haemorrhagic shock was induced by blood drawing, and then resuscitation was obtained by infusion of shed blood and two-fold volume saline. Results: Histological findings, as well as assays of neutrophilic infiltration (myeloperoxidase activity, ICAM-1 expression), inflammatory cytokines and pro-inflammatory factor (I kappa B-alpha and NF-kappa B p65) confirmed that haemorrhagic shock induced acute lung injury. BML-111 significantly mitigated acute lung injury induced by haemorrhagic shock. However, BOC-2, an antagonist of the lipoxinA4-receptor, partially reversed the protective effect of BML-111 on the haemorrhagic shock-induced the acute lung injury. Conclusion: BML-111 protects haemorrhagic shock-induced acute lung injury in rats. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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