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Coagulation-dependent mechanisms and asthma
Michael A. Matthay, John A. Clements
Michael A. Matthay, John A. Clements
Published July 1, 2004
Citation Information: J Clin Invest. 2004;114(1):20-23. https://doi.org/10.1172/JCI22288.
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Commentary

Coagulation-dependent mechanisms and asthma

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Abstract

In several clinical disorders, there are interactions between inflammation-dependent tissue injury and thrombin formation, fibrin deposition, and impaired fibrinolysis. New evidence generated from a mouse model of allergic airway hyperreactivity suggests that disordered coagulation and fibrinolysis may contribute to the pathogenesis of asthma . The inflammatory mechanisms that lead to airway smooth muscle contraction and airway hyperresponsiveness may be associated with accumulation of extravascular fibrin, plasma exudates, and inflammatory cells that can lead to airway closure.

Authors

Michael A. Matthay, John A. Clements

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Figure 2

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Schematic cross-sectional diagram of terminal airways illustrating the t...
Schematic cross-sectional diagram of terminal airways illustrating the transition from an opened to a closed airway. Contraction of smooth muscle cells favors airway constriction coupled with variable quantities of plasma proteins in the airway wall and the airway lumen, including fibrin deposition (see Figure 1 in Wagers et al. [ref. 6]). Normally there are tethering forces that will tend to expand terminal airways, while the quantity and quality of airway liquid (and mucus) favor airway obstruction. Although surface tension in the distal airways would be expected to play a minor role in decreasing patency under these conditions, administration of exogenous surfactant might help expel occluding material by dilution, dispersion, and rapid lowering of surface tension at the surfaces of the plugs.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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