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Clinical Investigations

Bronchial Hyperresponsiveness and Exhaled Nitric Oxide in Patients with Cardiac Disease

Nishimura Y. · Yu Y. · Kotani Y. · Nishiuma T. · Lin S. · Maeda H. · Yokoyama M.

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First Department of Internal Medicine, Kobe University School of Medicine, Kobe, Japan

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Respiration 2001;68:41–45

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Article / Publication Details

First-Page Preview
Abstract of Clinical Investigations

Published online: February 14, 2001
Issue release date: January – February

Number of Print Pages: 5
Number of Figures: 1
Number of Tables: 1

ISSN: 0025-7931 (Print)
eISSN: 1423-0356 (Online)

For additional information: https://www.karger.com/RES

Abstract

Background: Increased concentrations of exhaled nitric oxide (NO) correlate with increased airway inflammation and measurement of exhaled NO is a noninvasive method for the management of bronchial asthma. In various cardiac diseases, bronchial hyperresponsiveness is observed, as is bronchial asthma. However, there have been few studies on the relationship between exhaled NO and bronchial responsiveness in cardiac diseases. Objective: The aim of this study was to clarify the association between exhaled NO and bronchial hyperresponsiveness in patients with cardiac disease. Methods: We measured expired NO and bronchial responsiveness to inhaled methacholine in 19 patients with cardiac diseases and 17 with bronchial asthma. We divided the cardiac disease patients into two groups according to their bronchial responsiveness to inhaled methacholine: BHR(+) group consisted of 12 patients with bronchial hyperresponsiveness and BHR(–) group consisted of 7 patients without bronchial hyperresponsiveness. Results: The concentration of exhaled NO in the asthmatic patients was significantly higher than that in the BHR(+) and BHR(–) groups (142.0 ± 17.0, 33.6 ± 6.4 and 42.3 ± 10.3 ppb, respectively, p < 0.01). There was no significant difference in exhaled NO between BHR(+) and BHR(–) groups. There were also no significant differences in the parameters of bronchial hyperresponsiveness between the cardiac BHR(+) and bronchial asthma groups. These results indicate that bronchial hyperresponsiveness in patients with cardiac diseases is not a consequence of eosinophilic inflammation or of exhaled NO. Conclusion: We conclude that bronchial hyperresponsiveness in patients with cardiac diseases can occur independently of NO production.

© 2001 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Clinical Investigations

Published online: February 14, 2001
Issue release date: January – February

Number of Print Pages: 5
Number of Figures: 1
Number of Tables: 1

ISSN: 0025-7931 (Print)
eISSN: 1423-0356 (Online)

For additional information: https://www.karger.com/RES


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