Abstract
Background: Endothelial microparticles (EMPs) are produced by activated or apoptotic cells during various human and experimental disease states. Previous experimental work in our lab has shown that exogenous EMPs injected into a murine model cause a significant increase in pulmonary capillary permeability, induce oxidative injury in the respiratory epithelium and vasculature, and inhibit endothelium-mediated vasodilatation and nitric oxide production. Myeloperoxidase (MPO) has been implicated in the propagation of lung injury through the products formed as part of the MPO-mediated antimicrobial system.
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