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It is still uncertain how viral respiratory infections cause acute exacerbations of bronchial asthma, although several mechanisms have been proposed. We studied the relationship between the airway narrowing and the inflammatory and bronchospastic factors in peripheral venous blood and urine, in 30 patients with asthma at the exacerbations caused by upper respiratory tract infections (URTIs). Acute exacerbations caused decreases in peak expiratory flow rate (PEFR) in all 30 patients with asthma. Asthma exacerbations caused the rises in serum levels of interleukin-6, soluble intercellular adhesion molecule-1 and eosinophil cationic protein, concentrations of urinary leukotriene E4 and plasma histamine, compared with those in patients with asthma at a stable condition and those in 30 control subjects (p < 0.05). The values of PEFR at the exacerbations correlated with the levels of these factors. Treatment with oral glucocorticoids reversed the decreases in PEFR and the increases in these factors. At the onset of URTIs, rhinovirus and influenza type A virus were identified in 13 and 7 patients, respectively. Each of parainfluenza virus, adenovirus, and enterovirus was identified in one patient. These findings suggest that respiratory viral infections may cause acute asthma exacerbations via the production of mediators that induce inflammation and bronchospasm.

Exhaled carbon monoxide (CO) concentrations were measured on a CO monitor by vital capacity maneuvers in asthmatic patients receiving or not receiving inhaled corticosteroids and in nonsmoking and smoking healthy control subjects. CO was detectable and measured reproducibly in the exhaled air of all subjects. The exhaled CO concentrations were higher in asthmatic patients not receiving inhaled corticosteroids (5.6+/-0.6 ppm, p < 0.001) and similar in asthmatic patients receiving inhaled corticosteroids (1.7+/-0.1 ppm) compared with those in nonsmoking healthy control subjects (1.5+/-0.1 ppm). Smoking healthy control subjects had the highest levels of exhaled CO concentration among the groups (21.6+/-2.8 ppm, p < 0.001). To examine whether inhaling corticosteroids reduce exhaled CO concentration in a given asthmatic patient, 12 patients with symptomatic asthma who were being treated by inhaled beta2-agonists alone underwent measurements of exhaled CO concentration before and 4 wk after the initiation of inhaled corticosteroid treatment. All patients had reductions in exhaled CO concentration (p < 0.001) and eosinophil cell counts in sputum (p < 0.01) that were accompanied by an improvement in airway obstruction. Changes in exhaled CO concentration were significantly related to those in the eosinophil cell counts in sputum (p < 0.001). The present study shows an elevation of exhaled CO in asthmatic patients that decreases with corticosteroid therapy. Increases in the exhaled CO levels therefore may reflect inflammation in the asthmatic lung.

To study the cytoplasmic motility (CM) of alveolar macrophages (AM) during immediate asthmatic response, we measured remanent filed strength (RFS) in dogs in vivo after Ascaris suum-antigen (AA) inhalation. Four days after instillation of ferrimagnetic particles (Fe3O4, 3 mg/kg) into the right lower lobe bronchus, RFS was measured at the body surface immediately after magnetization of the Fe3O4 particles by an externally applied magnetic field. RFS decreased with time because of particle rotation (relaxation). Relaxation is thought to be correlated to CM of AM (J. Appl. Physiol. 55: 1196-1202, 1983). AA inhalation increased respiratory resistance (Rrs) in 10 dogs (responders; P less than 0.01), and did not change Rrs in five dogs (nonresponders; P greater than 0.50). The relaxation rate (lambda 0) significantly decreased because of AA inhalation in responders (P less than 0.01), whereas lambda 0 did not change in nonresponders (P greater than 0.50). Intravenous injection of indomethacin or diclofenac sodium (5 mg/kg) 30 min before AA inhalation completely inhibited the decrease in lambda 0 induced by AA inhalation, although both drugs did not inhibit the increase in Rrs (P greater than 0.10). In in vitro experiments, AM (5 x 10(6) cells) cells) harvested by bronchoalveolar lavage showed a significant dose-dependent decrease in lambda 0 with prostaglandins (PG) E1 and E2. However, histamine and platelet-activating factor increased lambda 0 significantly (P less than 0.01), whereas PGD2, PGF2 alpha, PGI2, thromboxane A2, leukotrienes B4, C4, and D4, and AA itself were without effect (P greater than 0.50). Furthermore, PGE2 aerosols mimicked AA-induced effects on AM.(ABSTRACT TRUNCATED AT 250 WORDS)