American Review of Respiratory Disease · 1993 · 307 citations · 34 references
AsthmaInflammatory Lung DiseaseLung InflammationEosinophilic DisorderPulmonary PharmacologyNebulized AdenosineAdenosine ConcentrationsLung DepositionAllergyPulmonary MedicineBal Adenosine ConcentrationsPharmacologyPulmonary DiseaseInhalation ToxicologyPhysiologyPulmonary PhysiologyLung MechanicsBronchoalveolar Lavage FluidMedicine
The inhalation of nebulized adenosine causes bronchoconstriction in asthmatics. In order to explore whether endogenously produced adenosine may contribute to the pathophysiologic aspects of asthma, we measured adenosine concentrations in bronchoalveolar lavage (BAL) fluid in seven subjects with asthma, eight asymptomatic cigarette smokers, and eight normal subjects. The mean concentration of adenosine in BAL fluid from the normal subjects was 0.72 +/- 0.16 microM. Subjects with asthma and cigarette smokers had significantly increased concentrations of adenosine in BAL fluid, 2.55 +/- 0.50 and 1.89 +/- 0.50 microM, respectively. Corrected for the dilution that occurs as a result of the lavage procedure, mean epithelial lining fluid adenosine concentrations were 60 +/- 13 microM in normal subjects, 193 +/- 58 microM in asthmatics, and 155 +/- 56 microM in smokers. Adenosine concentrations were positively correlated with the protein content of the lavage fluid (r = 0.79). Inhalation of nebulized adenosine in the subjects with asthma provoked a 20% reduction in lung function at concentrations 4- to 195-fold higher than was present in the epithelial lining fluid of the same individuals. The presence of increased BAL adenosine concentrations in asthmatics and in cigarette smokers suggests that adenosine may be a nonspecific marker for inflammation in the lung. The demonstration of physiologically relevant concentrations of adenosine in airway fluids of subjects with bronchial hyperreactivity to inhaled adenosine provides evidence for a role of endogenous adenosine in provoking bronchoconstriction in asthma.
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Changes in the normal maximal expiratory flow-volume curve with growth and aging.
Ronald J. Knudson, M D Lebowitz, Catharine J. Holberg et al. · PubMed · 1983 · 1.9K citations
Sven‐Erik Dahlén, Göran K. Hansson, Per Hedqvist et al. · Proceedings of the National Academy of Sciences · 1983 · 420 citations · Full text
Asthma, Environmental Allergy, Inflammatory Lung Disease +17