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Airway responsiveness to adenosine 5'-monophosphate in chronic obstructive pulmonary disease is determined by smoking.
Am Rev Respir Dis. 1993 Mar; 147(3):553-8.AR

Abstract

In contrast to methacholine, a stimulus that induces airway constriction mainly by "direct" stimulation of airway smooth muscle cells, AMP airway responsiveness reflects "indirectly" induced airway narrowing via inflammatory or neural reflex mechanisms. In order to determine inflammatory contribution to airway narrowing in COPD, we performed AMP and methacholine inhalation provocation tests in nonatopic subjects with COPD and compared the results with those obtained from atopic nonsmoking asthmatics and from healthy smoking volunteers. AMP caused airway narrowing in all but two subjects with COPD and in only three of the 12 healthy smoking subjects. Patients with COPD were significantly more responsive to AMP and methacholine than were healthy smoking volunteers. Geometric mean PC20 AMP was significantly lower in the smokers with COPD (7.2 mg/ml) than in the nonsmokers with COPD (58.5 mg/ml), whereas PC20 methacholine values and baseline FEV1 were comparable. In the nonatopic nonsmoking subjects with COPD, PC20 AMP was significantly higher than in the atopic nonsmoking asthmatics (3.8 mg/ml), whereas they responded similar to methacholine provocation. These results indicate that most subjects with COPD respond to AMP provocation and that smoking determines the degree of airway responsiveness to AMP in COPD. We suggest that increased susceptibility to mediator release by mast cells or neural reflex mechanisms are involved in AMP-induced airway constriction in asthma and in COPD.

Authors+Show Affiliations

Department of Pulmonology, University Hospital, Groningen, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8442586

Citation

Oosterhoff, Y, et al. "Airway Responsiveness to Adenosine 5'-monophosphate in Chronic Obstructive Pulmonary Disease Is Determined By Smoking." The American Review of Respiratory Disease, vol. 147, no. 3, 1993, pp. 553-8.
Oosterhoff Y, de Jong JW, Jansen MA, et al. Airway responsiveness to adenosine 5'-monophosphate in chronic obstructive pulmonary disease is determined by smoking. Am Rev Respir Dis. 1993;147(3):553-8.
Oosterhoff, Y., de Jong, J. W., Jansen, M. A., Koëter, G. H., & Postma, D. S. (1993). Airway responsiveness to adenosine 5'-monophosphate in chronic obstructive pulmonary disease is determined by smoking. The American Review of Respiratory Disease, 147(3), 553-8.
Oosterhoff Y, et al. Airway Responsiveness to Adenosine 5'-monophosphate in Chronic Obstructive Pulmonary Disease Is Determined By Smoking. Am Rev Respir Dis. 1993;147(3):553-8. PubMed PMID: 8442586.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Airway responsiveness to adenosine 5'-monophosphate in chronic obstructive pulmonary disease is determined by smoking. AU - Oosterhoff,Y, AU - de Jong,J W, AU - Jansen,M A, AU - Koëter,G H, AU - Postma,D S, PY - 1993/3/1/pubmed PY - 1993/3/1/medline PY - 1993/3/1/entrez SP - 553 EP - 8 JF - The American review of respiratory disease JO - Am Rev Respir Dis VL - 147 IS - 3 N2 - In contrast to methacholine, a stimulus that induces airway constriction mainly by "direct" stimulation of airway smooth muscle cells, AMP airway responsiveness reflects "indirectly" induced airway narrowing via inflammatory or neural reflex mechanisms. In order to determine inflammatory contribution to airway narrowing in COPD, we performed AMP and methacholine inhalation provocation tests in nonatopic subjects with COPD and compared the results with those obtained from atopic nonsmoking asthmatics and from healthy smoking volunteers. AMP caused airway narrowing in all but two subjects with COPD and in only three of the 12 healthy smoking subjects. Patients with COPD were significantly more responsive to AMP and methacholine than were healthy smoking volunteers. Geometric mean PC20 AMP was significantly lower in the smokers with COPD (7.2 mg/ml) than in the nonsmokers with COPD (58.5 mg/ml), whereas PC20 methacholine values and baseline FEV1 were comparable. In the nonatopic nonsmoking subjects with COPD, PC20 AMP was significantly higher than in the atopic nonsmoking asthmatics (3.8 mg/ml), whereas they responded similar to methacholine provocation. These results indicate that most subjects with COPD respond to AMP provocation and that smoking determines the degree of airway responsiveness to AMP in COPD. We suggest that increased susceptibility to mediator release by mast cells or neural reflex mechanisms are involved in AMP-induced airway constriction in asthma and in COPD. SN - 0003-0805 UR - https://www.unboundmedicine.com/medline/citation/8442586/Airway_responsiveness_to_adenosine_5'_monophosphate_in_chronic_obstructive_pulmonary_disease_is_determined_by_smoking_ L2 - https://www.atsjournals.org/doi/10.1164/ajrccm/147.3.553?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -