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Resuscitation. 2012 Jul;83(7):907-12. doi: 10.1016/j.resuscitation.2011.12.035. Epub 2012 Jan 12.

BML-111, a lipoxin receptor agonist, protects haemorrhagic shock-induced acute lung injury in rats.

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1
Department of Anesthesiology and Critical Care, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Abstract

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 (IκB-α and NF-κB 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 lipoxinA(4)-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.

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