Reactive airways dysfunction syndrome presenting as a reversible restrictive defect

Lung ◽  
1989 ◽  
Vol 167 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Robert Gilbert ◽  
J. Howland Auchincloss
Keyword(s):  
Restrictive Defect ◽  
Reactive Airways

A Case of Reactive Airways Dysfunction Syndrome in a Synthetic Resin Manufacture Factory

2008 ◽  
Vol 20 (4) ◽  
pp. 372
Author(s):  
So Young Park ◽  
Jong Seong Lee ◽  
Boo Wook Kim ◽  
Joung Oh Lee ◽  
Kyu Chul Park ◽  
...  
Keyword(s):  
Synthetic Resin ◽  
Reactive Airways

Restrictive Defect in Klinefelter's Syndrome

CHEST Journal ◽  
1982 ◽  
Vol 82 (1) ◽  
pp. 132 ◽  
Author(s):  
Basil Varkey ◽  
Akira Funahashi
Keyword(s):  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Restrictive Defect

Clinical Manifestations, Management, and Natural Course of Infants with Recurrent Bronchiolitis or Reactive Airways Disease

2014 ◽  
Vol 21 (1) ◽  
pp. 37 ◽  
Author(s):  
Hyoun Jin Park ◽  
Joo Hyun Kim ◽  
Yoon Hong Chun ◽  
Soo Young Lee ◽  
Sang Yong Kim ◽  
...  
Keyword(s):  
Clinical Manifestations ◽  
Natural Course ◽  
Reactive Airways

Reactive Airways Dysfunction Syndrome and Irritant-Induced Asthma

2006 ◽  
pp. 581-629 ◽  
Author(s):  
Denyse Gautrin ◽  
Stuart Brooks ◽  
Paul Henneberger
Keyword(s):  
Reactive Airways

Inflammation and cell-cell interactions in airway hyperresponsiveness

1991 ◽  
Vol 260 (4) ◽  
pp. L189-L206 ◽  
Author(s):  
A. R. Leff ◽  
K. J. Hamann ◽  
C. D. Wegner
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Difficult Problem ◽  
Experimental Models ◽  
Cytotoxic Effects ◽  
Epithelial Secretion ◽  
Eosinophil Granule ◽  
Conducting Airways ◽  
Reactive Airways

Airway hyperresponsiveness results from the conversion of normally reactive airways to a state of augmented responsiveness to constrictor stimuli. Although the mechanism accounting for the induction of airway hyperresponsiveness remains elusive, recent investigations have suggested that inflammation may be a sine qua non for human asthma. Numerous experimental models have demonstrated the necessity of circulating granulocytes as mediators of augmented bronchoconstriction during immune challenge. It is not known how granulocytes are targeted for selective migration to the conducting airways of the lung during hyperresponsive states; however, recent evidence implicates the upregulation of granulocyte adhesion molecules on both the endothelial and epithelial surfaces of the airway. There is evidence that during migration diapedesis, granulocytes interact with epithelial and endothelial cells to produce regionally secreted mediators that upregulate the responsiveness of adjacent airway smooth muscle and/or cause lumenal edema, thus augmenting the effect of constrictor stimuli. Most evidence suggests that the eosinophil is the most important granulocyte in these responses and that eosinophilic infiltration and activation may account for the unique, spasmodic, and cyclic nature of hyperreactive airways. The molecular biology of the eosinophil granule proteins has characterized four distinct substances, each of which exerts potential cytotoxic effects on airway epithelium by different mechanism. In addition, at least one of these proteins, the major basic protein, appears to cause direct, noncytotoxic stimulation of epithelial secretion that upregulates nonspecifically the response of airway smooth muscle to contractile stimuli. The recognition of inflammation as the essential component to airway hyperresponsiveness provides a fresh approach to a difficult problem and suggests a host of novel therapies for human asthma.

scholarly journals Chronic rhinitis in workers at risk of reactive airways dysfunction syndrome due to exposure to chlorine

1999 ◽  
Vol 56 (5) ◽  
pp. 334-338 ◽  
Author(s):  
C. Leroyer ◽  
J. L. Malo ◽  
D. Girard ◽  
J. G. Dufour ◽  
D. Gautrin
Keyword(s):  
At Risk ◽  
Chronic Rhinitis ◽  
Reactive Airways
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