Tuberc Respir Dis.  2001 Dec;51(6):503-516. 10.4046/trd.2001.51.6.503.

Phospholipase A2 Contributes to Hemorrhage-induced Acute Lung Injury Through Neutrophilic Respiratory Burst

Abstract

BACKGROUND
The present study was carried out in association with neutrophilic respiratory burst in the lung in order to clarify the pathogenesis of acute respiratory distress syndrome(ARDS) following acute severe hemorrhage. Because oxidative stress has been suggested as one of the principal factors causing tissue injury, the role of free radicals from neutrophils was assessed in acute hemorrhage-induced lung injury. METHOD: In Sprague-Dawley rats, hemorrhagic shock was induced by withdrawing blood(20 ml/kg of B.W) for 5 min and the hypotensive state was sustained for 60 min. To determine the mechanism and role of oxidative stress associated with phospholipase A2(PLA2) by neutrophils, the level of lung leakage, pulmonary myeloperoxidase(MPO), and the pulmonary PLA2 were measured. In addition, the production of free radicals was assessed in isolated neutrophils by cytochemical electron microscopy in the lung.
RESULTS
In hypotensive shock-induced acute lung injury, the pulmonary MPO, the level of lung leakage and the production of free radicals were higher. The inhibition of PLA2 with mepacrine decreased the pulmonary MPO, level of lung leakage and the production of free radicals from neutrophils.
CONCLUSION
A. neutrophilic respiratory burst is responsible for the oxidative stress causing acute lung injury followed by acute, severe hemorrhage. PLA2 activation is the principal cause of this oxidative stress.

Keyword

Acute hemorrhage; ARDS; Oxidative stress; PLA2

MeSH Terms

Acute Lung Injury*
Free Radicals
Hemorrhage
Lung
Lung Injury
Microscopy, Electron
Neutrophils*
Oxidative Stress
Phospholipases A2*
Phospholipases*
Quinacrine
Rats, Sprague-Dawley
Respiratory Burst*
Shock, Hemorrhagic
Free Radicals
Phospholipases
Phospholipases A2
Quinacrine
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