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Pharmacomechanical hyperresponsiveness in ozone-induced airway injury.

Murlas-CG

NIOSH 1993 Mar; :1-6

20023647

Our current research aims to determine in vivo and in vitro mechanisms which increase airway responsiveness. This has and will continue to be done in subjects with bronchial hyperreactivity, the increased airway irritability which characterizes asthma and ozone-induced lung injury. What we have learned from our previous studies of airway structure and function in this disorder suggests that injury to normal lung constituents results in the elaboration of factors leading to cholinergic neuromuscular hyperresponsiveness. Among the many potential cell types that could influence bronchomotor tone are cells of the respiratory mucosa which may affect airway muscle both pre- and post-synaptically. From our work, it appears that airway muscle responsiveness in acute, ozone-induced bronchial hyperreactivity is increased, and that this hyperresponsiveness is linked to more than one noncyclooxygenase. mucosa-derived factor in the guinea pig. Thus, we speculate that the hyperreactivity developing acutely after ozone exposure may be due to mucosa-derived factors and the cellular mechanisms by which they augment smooth muscle contractility merit further study.

In-vitro-studies; In-vivo-studies; Bronchial-asthma; Hypersensitivity; Occupational-respiratory-disease; Airway-obstruction; Cholinergic-receptors; Cell-damage; Muscles; Pulmonary-function; Pulmonary-system-disorders; Respiratory-system-disorders; Lung-disease

Rush-Presbyterian St. Luke Medical Center, Department of Medicine (Pulmonary), 1653 W. Congress Parkway, Chicago, IL 60612

10028-15-6

19930301

Final Grant Report

127961

Grant

1993

Grant-Number-K01-OH-00060

OEP

Pulmonary-system-disorders

National Institute for Occupational Safety and Health

IL

Rush-Presbyterian St. Luke Medical Center, Department of Medicine (Pulmonary), Chicago, IL 60612