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1 Dept of Respiratory Medicine, Royal Prince Alfred Hospital, Camperdown, Australia. 2 Div for Experimental Asthma & Allergy Research, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. 3 Dept of Pharmacy, University of Sydney, Sydney, Australia
CORRESPONDENCE: S.D. Anderson, Dept of Respiratory Medicine, E11S, Royal Prince Alfred Hospital, Missenden Road, Camperdown, Australia. Fax: 61 295158196. E-mail: sandya@mail.med.usyd.edu.au
Keywords: bronchial provocation, leukotriene E4, mannitol, N
-methylhistamine, 9
, 11ß-prostaglandin F2, urinary mediators
Received: January 30, 2003
Accepted April 9, 2003
This study was supported by the National Health and Medical Research Council of Australia (J.D. Brannan), the Swedish Medical Research Council (12754, 13047, 9072), the Swedish Society for Health Care and Allergy Research (Vårdalstiftelsen), the Swedish Heart Lung Foundation, the Swedish Asthma and Allergy Research Foundation and Karolinska Institutet.
The aim of this study was to investigate if mannitol inhalation, as a model of exercise-induced bronchoconstriction (EIB), causes mast cell activation and release of mediators of bronchoconstriction.
Urinary excretion of previously identified mediators of EIB was investigated in association with mannitol-induced bronchoconstriction. Twelve asthmatic and nine nonasthmatic subjects inhaled mannitol and urine was collected 60 min before andfor90 min after challenge. The urinary concentrations of leukotriene (LT)E4, the prostaglandin (PG)D2 metabolite and the mast cell marker 9
In asthmatic subjects, inhalation of a mean±sem dose of 272±56 mg mannitol induced a reduction in forced expiratory volume in one second (FEV1) of 34.5±2.1%. This was associated with increases in urinary 9
The increased urinary levels of 9
,11ß-PGF2 weremeasured by enzyme immunoassay. N-methylhistamine was measured by radioimmunoassay. ,11ß-PGF2 (91.9±8.2 versus 66.9±6.6 ng·mmol creatinine–1, peak versus baseline) and LTE4 (51.3±7.5 versus 32.9±4.7). In nonasthmatic subjects, the reduction in FEV1 was 1.0±0.5% after inhaling 635 mg of mannitol. Although smaller than in the asthmatics, significant increases of urinary 9,11ß-PGF2 (68.4±6.9 versus 56.0±5.8 ng·mmol creatinine–1) and LTE4 (58.5±5.3 versus 43.0±3.3 ng·mmol creatinine–1) were observed in the nonasthmatic subjects. There was also a small increase in urinary excretion of N-methylhistamine in the nonasthmatics, but not in the asthmatics. ,11ß-prostaglandin F2 support mast cell activation with release of mediators following inhalation of mannitol. Increased bronchial responsiveness to the released mediators could explain the exclusive bronchoconstriction in asthmatic subjects.
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