Journal
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
Volume 118, Issue 2, Pages 72-82Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/13813455.2012.665463
Keywords
Ischemia-reperfusion; oxidative stress; nitric oxide synthase; fibrinogen
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Context: Platelets have significant roles in initiating and mediating reduced alveolar blood flow, microvascular leak, and ventilation/perfusion mismatch caused by metabolic changes and altered signal transduction caused by ischemia-reperfusion. Objective: This review focuses on platelet mechanisms of vascular dysfunction in the lung and presents a hypothesis for interplay between platelet activation, endothelial damage and fibrinogen. The purpose is to discuss current knowledge regarding mechanisms of platelet-mediated endothelial injury and implications for new strategies to treat vascular dysfunction associated with acute lung injury (ALI). Methods: Literature from a number of fields was searched using Medline and Google Scholar. Results: Activated platelets contribute to redox imbalance through reactive oxygen species production, pro-leak molecules such as PAF and serotonin, and recruitment of inflammatory cytokines and leukocytes to the damaged endothelium. Conclusion: Platelets are a critical component of pulmonary ALI, acting in conjunction with fibrinogen to mediate endothelial damage through multiple signal transduction pathways.
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