Determinants of the bronchodilation response to salbutamol on histamine-induced bronchoconstriction.

Assessment of the bronchodilation response to short-acting beta2-adrenoreceptor agonists on pharmacologically induced bronchoconstriction has often been used to investigate airway smooth muscle beta2-adrenoreceptor function. However, little is known about factors affecting this response. In the present study, the bronchodilation response to 0.2 mg of salbutamol on histamine-induced bronchoconstriction was assessed in 101 steroid-naïve asthmatic subjects. The associations of the response with a wide range of challenge procedure-related variables, clinical asthma severity indicators, and blood markers of airway inflammation were investigated. The response was re-assessed after 6 and 12 weeks' therapy with inhaled budesonide. Baseline FEV1, final histamine concentration, and the maximal fall in FEV1 explained 35-59% of the total variation in the response to salbutamol, depending on the index chosen to express the response. Serum concentration of myeloperoxidase, an index of neutrophilic inflammation, was associated with a poor response. The preceding week daily PEF variation, rescue bronchodilator use, severity of asthmatic symptoms, blood eosinophil count, and serum eosinophilic cationic protein and eosinophilic protein X concentrations were not associated with the response. The salbutamol response seemed to diminish during budesonide treatment but when adjusted by the challenge procedure-related variables the treatment effect vanished. In conclusion, the bronchodilation response to salbutamol on histamine-induced bronchoconstriction is largely determined by challenge procedure-related variables. It seems to be unrelated to the clinical severity of asthma and is not affected by treatment with inhaled corticosteroids. Neutrophilic airway inflammation may be associated with a poor response.

Delaying decline in pulmonary function with physical activity: a 25-year follow-up.

The importance of physical activity for health is well recognized, but little is known about the influence of physical activity on pulmonary function. We have examined whether physical activity could slow down the decline in pulmonary function among the southwestern rural Finnish cohort of the Seven Countries Study. Physical activity was estimated by kilometers walked, cycled, and skied daily. We had complete data for 429 men for 10 years, 275 men for 20 years, and 186 men for 25 years. During the first 10 years, the decline in FEV was 9.8 ml/year less among men in the highest tertile of baseline physical activity than in men in the lowest tertile. According to the mean physical activity over either 20 or 25 years, men in the highest tertile also lost less pulmonary function (p = 0.009 and p = 0.043, respectively). A similar beneficial effect was observed in all smoking categories. In mortality analysis, continued high physical activity and an increase in activity to high level were associated with lower mortality. In conclusion, results indicated that physical activity is associated with a slower decline in pulmonary function and with lower mortality, and thus, middle-aged and older people should be encouraged to enjoy exercise.