Airway function after cyclooxygenase inhibition during hyperpnea-induced bronchoconstriction in guinea pigs

Suman, Oscar E.; Morrow, Jason D.; O'Malley, K; Beck, Kenneth C.

doi:10.1152/jappl.2000.89.5.1971

Cited by 11 publications

(8 citation statements)

References 44 publications

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“…However, evidence for the bronchodilating effect of PGE 2 and decreased airway hyperresponsiveness after a second bout of exercise has been questioned. Suman et al [44] found decreased PGE 2 levels in lung lavage fluid from guinea pigs immediately after hyperventilation and found no evidence that PG involvement caused refractoriness to repeat hyperventilation.…”

Section: Discussionmentioning

confidence: 97%

Comparative Effects of a High-Intensity Interval Warm-Up and Salbutamol on the Bronchoconstrictor Response to Exercise in Asthmatic Athletes

Mickleborough¹,

Lindley²,

Turner³

2007

Int J Sports Med

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Approximately half of all asthmatics become refractory to exercise-induced bronchoconstriction (EIB) with repeated challenges. Exercise refractoriness has been utilized by asthmatic athletes to reduce the bronchoconstrictor response to exercise prior to competition, and this has led to the observation that some asthmatic athletes can "run through" their asthma. The main aim of this study was to investigate the efficacy of short high-intensity, repeated warm-ups compared with salbutamol (a commonly used inhaled beta (2)-agonist) on the severity of EIB. Eight moderately trained (.VO(2peak), 51.9 +/- 2.3 ml . kg (-1) . min (-1)) recreational asthmatic athletes with documented EIB were tested under 4 experimental conditions: 1) control (CON) condition; 2) an interval warm-up (WU) consisting of 8 x 30-sec runs at peak treadmill speed, with 45-sec recovery between each sprint; 3) inhaling 200 microg of salbutamol (Ventolin, GlaxoSmithKline, Uxbridge, Middlesex, U.K.) (IH); and 4) combining both the WU and IH session. All 4 experimental sessions were followed by an exercise challenge test (85-90 % predicted maximum heart rate for 8 min). Pulmonary function was measured pre-exercise and at 1, 5, 10, 15 min postexercise. The mean maximum percent fall in pre- to postexercise forced expiratory volume in 1-sec (FEV (1)) for all 8 asthmatic subjects during the EIB screening test (CON session) was - 18.25 +/- 4.01 %. The mean maximum percent decrease in postexercise FEV (1) significantly decreased (p < 0.05) to only - 9.1 +/- 0.6 % following the WU condition, which is below the EIB diagnostic threshold of a 10 % fall in postexercise FEV (1). The IH and WU + IH condition resulted in a substantial postexercise bronchodilation as shown by a significant increase (p < 0.05) in the mean maximum percent change in postexercise FEV (1) following the IH (+ 8.9 +/- 6.1 %) and WU + IH (+ 15.2 +/- 4.6 %) condition. Similar changes as a result of experimental condition were observed for FEF (25-75 %). These data indicate that repeated high-intensity warm-ups can lessen the bronchoconstrictor response to exercise. In addition, combining the interval warm-up with salbutamol prior to exercise resulted in substantial bronchodilation and conferred a greater protective effect against developing EIB than either intervention alone.

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Section: Discussionmentioning

confidence: 97%

Comparative Effects of a High-Intensity Interval Warm-Up and Salbutamol on the Bronchoconstrictor Response to Exercise in Asthmatic Athletes

Mickleborough¹,

Lindley²,

Turner³

2007

Int J Sports Med

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“…Potential smooth muscle relaxant mediators that are known to be present in airway tissue include prostaglandins (mainly PGE 2 ) and nitric oxide (NO). Our laboratory has shown in other studies that prostaglandins do not have a major influence on airway smooth muscle during exercise in humans (7) or during hyperventilation in guinea pigs (35). Similarly, NO synthase inhibition has little effect on the changes in airway function during hyperventilation in the guinea pig (33).…”

mentioning

confidence: 88%

Role of airway endogenous nitric oxide on lung function during and after exercise in mild asthma

Suman

Beck

2002

Journal of Applied Physiology

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We hypothesized that nitric oxide (NO), a known mild bronchodilator that can be released by several cell types within pulmonary airways, might protect airways during exercise in asthmatic subjects. We studied 17 individuals with documented exercise-induced asthma (screening exercise evaluation) on 2 study days: after treatment with inhaled NO synthase inhibitor N(G)-monomethyl-l-arginine (l-NMMA; 2 ml of 25 mg/ml mist) and after treatment with saline vehicle. Pulmonary resistance (Rl, esophageal manometry) rose and forced expiratory volume in 1 s fell more after l-NMMA compared with saline treatment, suggesting a bronchoprotective role for NO at baseline. The rise in Rl seen after l-NMMA treatment was nearly completely reversed early in exercise, suggesting a non-NO-mediated bronchodilation. A slow rise in Rl during constant-load exercise and dramatic increase in Rl after exercise were the same on the 2 treatment days, indicating little role for NO in regulating airway function during and after exercise. We conclude that endogenous NO plays little role in regulating airway function during and after exercise in subjects with mild asthma.

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“…respiratory system resistance; asthma; exercise-induced asthma AIRWAY FUNCTION DURING EXERCISE or isocapnic hyperventilation (HV) is relatively well preserved in asthmatic subjects (3,5,44) as well as in guinea pigs (35,37), despite likely changes in airway fluid content that occur with hyperpnea. When airway function deteriorates during hyperpnea, it does so with a lesser magnitude compared with that seen in the posthyperpneic period.…”

mentioning

confidence: 99%

Role of nitric oxide during hyperventilation-induced bronchoconstriction in the guinea pig

Suman

Beck

2001

Journal of Applied Physiology

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Airway function is largely preserved during exercise or isocapnic hyperventilation in humans and guinea pigs despite likely changes in airway milieu during hyperpnea. It is only on cessation of a hyperpneic challenge that airway function deteriorates significantly. We tested the hypothesis that nitric oxide, a known bronchodilator that is produced in the lungs and bronchi, might be responsible for the relative bronchodilation observed during hyperventilation (HV) in guinea pigs. Three groups of anesthetized guinea pigs were given saline and three groups given 50 mg/kg N(G)-monomethyl-L-arginine (L-NMMA), a potent nitric oxide synthase inhibitor. Three isocapnic ventilation groups included normal ventilation [40 breaths/min, 6 ml/kg tidal volume (VT)], increased respiratory rate only (150 breaths/min, 6 ml/kg VT), and increased respiratory rate and increased volume (100 breaths/min, 8 ml/kg VT). L-NMMA reduced expired nitric oxide in all groups. Expired nitric oxide was slightly but significantly increased by HV in the saline groups. However, inhibition of nitric oxide production had no significant effect on rate of rise of respiratory system resistance (Rrs) during HV or on the larger rise in Rrs seen 6 min after HV. We conclude that nitric oxide synthase inhibition has no effect on changes in Rrs, either during or after HV in guinea pigs.

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Airway function after cyclooxygenase inhibition during hyperpnea-induced bronchoconstriction in guinea pigs

Cited by 11 publications

References 44 publications

Comparative Effects of a High-Intensity Interval Warm-Up and Salbutamol on the Bronchoconstrictor Response to Exercise in Asthmatic Athletes

Comparative Effects of a High-Intensity Interval Warm-Up and Salbutamol on the Bronchoconstrictor Response to Exercise in Asthmatic Athletes

Role of airway endogenous nitric oxide on lung function during and after exercise in mild asthma

Role of nitric oxide during hyperventilation-induced bronchoconstriction in the guinea pig

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