title: Exhaled nitric oxide decreases during exercise-induced bronchoconstriction in children with asthma.
abstract: Nitric oxide (NO) produced in the airways can be either detrimental or protective to the host. To investigate the role of NO in the pathogenesis of exercise-induced bronchoconstriction (EIB), we measured exhaled NO (ENO) after exercise challenge in 39 asthmatic and six normal children. FEV(1) and ENO were measured before and at 0, 5, 10, and 15 min after exercise performed on a treadmill for 6 min. EIB was defined as a decrease in FEV(1) of more than 15% after the exercise. Normal children (control group) did not have EIB. Twenty-one patients with asthma had EIB (EIB group) whereas the remaining 18 patients did not (non-EIB group). The baseline ENO value was significantly higher in the asthmatic children than in the normal children, and there was a positive correlation between the maximal percent decrease in FEV(1) and the baseline ENO value (r = 0.501, p = 0.012). At the end of the exercise, ENO had decreased in all the subjects. In the non-EIB and control groups, ENO rebounded to above the baseline at 5 min after the exercise and thereafter. In contrast, ENO remained at a decreased level in the EIB group. The change in ENO did not correlate with the change in minute ventilation, and beta-agonist inhalation at the peak of EIB that accelerated the recovery of FEV(1) did not affect the depressed level of ENO, demonstrating that the reduction of ENO is not a simple consequence of increased ventilation nor airway obstruction. Among the EIB group, steroid-treated patients showed sooner recovery in ENO after the exercise than steroid-naive patients. Our study suggests that NO production in response to exercise may be impaired in patients with EIB, and that ENO represents not only airway inflammation but also a protective function of NO in EIB.
authors.affiliation: Department of Pediatrics and Allergy, National Mie Hospital, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Terada
authors.forename: T
authors.initials: T
authors.lastname: Fujisawa
authors.forename: K
authors.initials: K
authors.lastname: Togashi
authors.forename: T
authors.initials: T
authors.lastname: Miyazaki
authors.forename: H
authors.initials: H
authors.lastname: Katsumata
authors.forename: J
authors.initials: J
authors.lastname: Atsuta
authors.forename: K
authors.initials: K
authors.lastname: Iguchi
authors.forename: H
authors.initials: H
authors.lastname: Kamiya
authors.forename: H
authors.initials: H
authors.lastname: Togari
mesh_terms: D000280:Administration, Inhalation; D000293:Adolescent; D000318:Adrenergic beta-Agonists / Q000494:pharmacology / Q000627:therapeutic use; D000704:Analysis of Variance; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001250:Asthma, Exercise-Induced / Q000175:diagnosis / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D001944:Breath Tests; D001993:Bronchodilator Agents / Q000494:pharmacology / Q000627:therapeutic use; D016022:Case-Control Studies; D002648:Child; D004359:Drug Therapy, Combination; D005080:Exercise Test; D005260:Female; D005541:Forced Expiratory Volume / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D009569:Nitric Oxide / Q000032:analysis* / Q000502:physiology*; D017265:Procaterol / Q000494:pharmacology / Q000627:therapeutic use; D013256:Steroids; D013997:Time Factors
chemical_list: D000318:Adrenergic beta-Agonists; D000893:Anti-Inflammatory Agents; D001993:Bronchodilator Agents; D013256:Steroids; D009569:Nitric Oxide; D017265:Procaterol