Irritant-induced asthma and reactive airways dysfunction syndrome

2013 ◽  
pp. 319-338
Keyword(s):  
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

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

scholarly journals Neuronal Modulation of Airway and Vascular Tone and Their Influence on Nonspecific Airways Responsiveness in Asthma

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Brendan J. Canning ◽  
Ariel Woo ◽  
Stuart B. Mazzone
Keyword(s):  
Nervous System ◽  
Smooth Muscle ◽  
Autonomic Nervous System ◽  
Vascular Tone ◽  
Autonomic Nerves ◽  
Substantial Body ◽  
Airways Hyperreactivity ◽  
Hallmark Feature ◽  
Reactive Airways ◽  
Airways Hyperresponsiveness

The autonomic nervous system provides both cholinergic and noncholinergic neural inputs to end organs within the airways, which includes the airway and vascular smooth muscle. Heightened responsiveness of the airways to bronchoconstrictive agents is a hallmark feature of reactive airways diseases. The mechanisms underpinning airways hyperreactivity still largely remain unresolved. In this paper we summarize the substantial body of evidence that implicates dysfunction of the autonomic nerves that innervate smooth muscle in the airways and associated vasculature as a prominent cause of airways hyperresponsiveness in asthma.

Pharmaceutical care program for patients with reactive airways disease

2001 ◽  
Vol 58 (9) ◽  
pp. 791-796 ◽  
Author(s):  
Morris Weinberger ◽  
Michael D. Murray ◽  
David G. Marrero ◽  
Nancy Brewer ◽  
Michael Lykens ◽  
...  
Keyword(s):  
Pharmaceutical Care ◽  
Care Program ◽  
Reactive Airways
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