Airways Reactivity in Patients with CF

2002 ◽  
Vol 23 (1) ◽  
pp. 077-086 ◽  
Author(s):  
Miles Weinberger
Keyword(s):  
1992 ◽  
Vol 13 (11) ◽  
pp. 403-412
Author(s):  
Gail G. Shapiro

Definition and Pathophysiology Asthma is a reversible airways disease characterized by both smooth muscle hyperreactivity and airway inflammation. During the 1970s and early 1980s the focus was on smooth muscle constriction, and it was believed that better bronchodilators would greatly diminish our difficulties in controlling this condition. This, unfortunately, was not the case. The emphasis of therapy today has turned to airway inflammation. Lung biopsies from patients who have asthma show destruction of respiratory epithelium, basement membrane thickening, and inflammatory cellular infiltrate. Among the infiltrating cells are eosinophils, macrophages, and neutrophils that are called to the site of inflammation by the chemotactic products released by activated mast cells. Upon their arrival, these cells release their own products of inflammation, which amplify this immunologic response. A variety of neuropeptides also play a role, some serving to stabilize and others to destabilize the airway. One result of this airway inflammation is airways reactivity, also known as bronchial hyperresponsiveness. A common example of this scenario is the child who has allergic asthma and encounters a problematic allergen. This child has immunoglobulin E (IgE) to this allergen bound to mast cells in his or her airway. Upon exposure to the allergen, the binding of IgE and antigen triggers mast cell mediator release within minutes.


1986 ◽  
Vol 61 (2) ◽  
pp. 640-646
Author(s):  
A. N. Freed ◽  
U. A. Scheffel ◽  
L. J. Kelly ◽  
B. Bromberger-Barnea ◽  
H. A. Menkes

Following ozone (O3) exposure, airways reactivity increases. We investigated the possibility that exposure to O3 causes a decrease in pulmonary perfusion, and that this decrease is associated with the increase in reactivity. Perfusion was measured with radiolabeled microspheres. A wedged bronchoscope was used to isolate sublobar segments in the middle and lower lobes of anesthetized dogs. Isolated segments were exposed to either O3 or an elevated alveolar pressure. Although increased alveolar pressure decreased microsphere density, exposure to 1 ppm O3 did not. Collateral system resistance rose significantly following exposure to O3 and to high pressure. These studies do not support the hypothesis that pulmonary perfusion is decreased following O3 exposure and is associated with subsequent increases in reactivity.


CHEST Journal ◽  
1984 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
W.C. Hodgson ◽  
D.J. Cotton ◽  
G.D. Werner ◽  
D.W. Cockcroft ◽  
J. A Dosman

Respiration ◽  
1996 ◽  
Vol 63 (4) ◽  
pp. 199-204 ◽  
Author(s):  
J.M. García-García ◽  
J.R. Hernández ◽  
M.A. Martínez-Muñiz ◽  
A. Sánchez-Antuña ◽  
M.G. Marrón ◽  
...  

1981 ◽  
Vol 15 ◽  
pp. 727-727 ◽  
Author(s):  
B G Nickerson ◽  
D B Bautista ◽  
M A Namey ◽  
W Richards ◽  
T G Keens

CHEST Journal ◽  
1982 ◽  
Vol 82 (1) ◽  
pp. 15-18 ◽  
Author(s):  
Marie Chatham ◽  
Eugene R. Bleecker ◽  
Philip Norman ◽  
Philip L. Smith ◽  
Pamela Mason

1991 ◽  
Vol 143 (6) ◽  
pp. 1322-1328 ◽  
Author(s):  
Jay Y. Westcott ◽  
Hunter R. Smith ◽  
Sally E. Wenzel ◽  
Gary L. Larsen ◽  
Rebecca B. Thomas ◽  
...  

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