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Role of Fibrin in Determining Airway Closure*

Scott Wagers, MD; Ryan Norton; Jason Bates, PhD; Charles G. Irvin, PhD
Author and Funding Information

*From the Vermont Lung Center, University of Vermont, Burlington, VT.

Correspondence to: Scott Wagers, MD, Rm 226, 149 Beaumont Ave, Burlington, VT 05405-0075; e-mail: scott.wagers@uvm.edu



Chest. 2003;123(3_suppl):362S-363S. doi:10.1378/chest.123.3_suppl.362S
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Airway fibrin deposition occurs in inflammatory disorders of the lung, and it is known that fibrin inhibits surfactant function. The pressure-volume (PV) curves of asthmatic patients are widened, and this is thought to be due to an enhancement of airway closure. Tissue plasminogen activator (tPA) is a fibrinolytic agent that works through the activation of plasminogen in the presence of fibrin. We sought to determine whether lysis of airway fibrin would diminish the PV curve widening that is seen in airway inflammation.

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