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Relationship between exhaled nitric oxide and airway hyperresponsiveness following experimental rhinovirus infection in asthmatic subjects.
Eur Respir J 1998; 11(1):126-32ER

Abstract

Exhaled nitric oxide (NO) is elevated in asthmatics, and varies with disease severity. We postulated that a respiratory virus infection increases exhaled NO levels in asthma, and examined the relationship between the virus-induced changes in exhaled NO and in airway hyperresponsiveness to histamine. In a parallel study, seven patients underwent experimental rhinovirus 16 (RV16) inoculation at days 0 and 1, whilst seven patients received placebo. Exhaled NO was measured at baseline (day 0) and at days 1, 2 and 3 after inoculation. Histamine challenges were performed prior to (day -7) and after inoculation (day 3), and were expressed as provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV1) (PC20). Following RV16 infection there was a significant increase in NO at days 2 and 3 as compared to baseline (median change (range): 4.2 (7.5) parts per billion (ppb), p=0.03, and 3.0 (10.1) ppb, p=0.02, respectively). Furthermore, PC20 decreased significantly following RV16 infection (mean+/-SD change in doubling dose: -0.65+/-0.54, p=0.02), whereas PC20 did not change in the placebo group (p=0.1). There was a significant correlation between the RV16-induced changes in exhaled NO levels at day 2 and the accompanying changes in PC20 at day 3 (rank correlation coefficient (rs): 0.86, p=0.01). Hence, the greater the increase in exhaled NO, the smaller the decrease in PC20. We conclude that rhinovirus infection increases exhaled nitric oxide levels in asthmatics, and that this increase is inversely associated with worsening of airway hyperresponsiveness to histamine. These results suggest that viral induction of nitric oxide synthase within the airways may play a protective role in exacerbations of asthma.

Authors+Show Affiliations

Dept of Pulmonology, Leiden University Medical Centre, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Controlled Clinical Trial
Journal Article

Language

eng

PubMed ID

9543281

Citation

de Gouw, H W., et al. "Relationship Between Exhaled Nitric Oxide and Airway Hyperresponsiveness Following Experimental Rhinovirus Infection in Asthmatic Subjects." The European Respiratory Journal, vol. 11, no. 1, 1998, pp. 126-32.
de Gouw HW, Grünberg K, Schot R, et al. Relationship between exhaled nitric oxide and airway hyperresponsiveness following experimental rhinovirus infection in asthmatic subjects. Eur Respir J. 1998;11(1):126-32.
de Gouw, H. W., Grünberg, K., Schot, R., Kroes, A. C., Dick, E. C., & Sterk, P. J. (1998). Relationship between exhaled nitric oxide and airway hyperresponsiveness following experimental rhinovirus infection in asthmatic subjects. The European Respiratory Journal, 11(1), pp. 126-32.
de Gouw HW, et al. Relationship Between Exhaled Nitric Oxide and Airway Hyperresponsiveness Following Experimental Rhinovirus Infection in Asthmatic Subjects. Eur Respir J. 1998;11(1):126-32. PubMed PMID: 9543281.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Relationship between exhaled nitric oxide and airway hyperresponsiveness following experimental rhinovirus infection in asthmatic subjects. AU - de Gouw,H W, AU - Grünberg,K, AU - Schot,R, AU - Kroes,A C, AU - Dick,E C, AU - Sterk,P J, PY - 1998/5/16/pubmed PY - 1998/5/16/medline PY - 1998/5/16/entrez SP - 126 EP - 32 JF - The European respiratory journal JO - Eur. Respir. J. VL - 11 IS - 1 N2 - Exhaled nitric oxide (NO) is elevated in asthmatics, and varies with disease severity. We postulated that a respiratory virus infection increases exhaled NO levels in asthma, and examined the relationship between the virus-induced changes in exhaled NO and in airway hyperresponsiveness to histamine. In a parallel study, seven patients underwent experimental rhinovirus 16 (RV16) inoculation at days 0 and 1, whilst seven patients received placebo. Exhaled NO was measured at baseline (day 0) and at days 1, 2 and 3 after inoculation. Histamine challenges were performed prior to (day -7) and after inoculation (day 3), and were expressed as provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV1) (PC20). Following RV16 infection there was a significant increase in NO at days 2 and 3 as compared to baseline (median change (range): 4.2 (7.5) parts per billion (ppb), p=0.03, and 3.0 (10.1) ppb, p=0.02, respectively). Furthermore, PC20 decreased significantly following RV16 infection (mean+/-SD change in doubling dose: -0.65+/-0.54, p=0.02), whereas PC20 did not change in the placebo group (p=0.1). There was a significant correlation between the RV16-induced changes in exhaled NO levels at day 2 and the accompanying changes in PC20 at day 3 (rank correlation coefficient (rs): 0.86, p=0.01). Hence, the greater the increase in exhaled NO, the smaller the decrease in PC20. We conclude that rhinovirus infection increases exhaled nitric oxide levels in asthmatics, and that this increase is inversely associated with worsening of airway hyperresponsiveness to histamine. These results suggest that viral induction of nitric oxide synthase within the airways may play a protective role in exacerbations of asthma. SN - 0903-1936 UR - https://www.unboundmedicine.com/medline/citation/9543281/Relationship_between_exhaled_nitric_oxide_and_airway_hyperresponsiveness_following_experimental_rhinovirus_infection_in_asthmatic_subjects_ L2 - http://erj.ersjournals.com/cgi/pmidlookup?view=long&pmid=9543281 DB - PRIME DP - Unbound Medicine ER -