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J Asthma Allergy Clin Immunol. 1998 Mar;18(1):40-51. Korean. Original Article.
Park JK , Bahn JW , Lee BJ , Son JW , Lee SR , Kim YK , Cho SH , Min KU , Kim YY .
Abstract

BACKGROUND: Exercise can aggravate asthmatic symptoms in many patients with bronchial asthma. It is caused by that inhaled air bypasses nasal cavity and goes directly to the lower airways through open mouth dring exercise. Although the pathogenetic mechanisms of exercise-induced asthma(EIA) have not been clarified yet, there is evidence that chemical mediators, released from the inflammatory cells triggered by airway cooling or drying, might be responsible for induction of bronchoconstriction. However, it has been controversial which chemical mediators or cells are involved in such process. Objectiye . The aim of this study was to evaluate the role of activated mast cells in the pathogenesis of EIA and find out whether or not sulfidopeptide leukotrienes (LTC4/d4/E4) are involved in the exercise-induced bronchoconstriction. MATERIAL AND METHOD: Eleven asthmatics with documented exercise-induced bronchoconstriction and 10 control subjects were studied. Before and 6 hours after free running for 6 minutes, forced expiratory volume in 1 second (FEV,) and the concentrations of N- methylhistamine, LTE4, and creatinine in unine collected for 6 hours after exercise were determined. RESULT: Urinary concentrations of N-methylhistamine(mean+SE, ng/mg creatinine) of EIA patients before and after exercise were 159+40 and 450+75, respectively. Those of control subjects were 208+ 54 and 275+ 62, respectively. Uninary N-methylhistamine levels of EIA group increased significantly after exercise, while those of control group did not change. Urinary concentrations of LTE,(mean+SE, pg/mg creatinine) of EIA patients before and after exercise were 15.6 k2.6 and 22.2+5.8, respectively. Those of control subjects were 10.4+ 4.0, 18.2 +7.0, respectively. The concentrations of LTE4 in the urine samples collected before exerise revealed no difference between EIA and control subjects (p=0.07). There was no change after exercise in both groups. Percent fall of FEV, was 29.1+8.0% (mean+SD) in EIA group and 3.4 + 4.0% in control group, respectively. There was no correlation between reduction of FEV, and change in urinary concentrations of N-methyl-histmine after exercise. CONCLUSTION: Chemical mediators of activated mast cells may be involved in exercise-induced bronchoconstriction, but there is little evidence for enhanced sulfidopeptide leukotriene generation as assessed by urinary LTE4.

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