We measured the frequency characteristics (at 10-40 Hz) of airway (Za) and tissue (Zt) impedances in cases of chronic obstructive pulmonary disease [asthmatic bronchitis (AB), chronic pulmonary emphysema (CPE)] and interstitial pneumonitis (IP) by use of an improved random noise oscillation and body box method. The results were then compared with those obtained for normal subjects. The real part of Za was markedly elevated in patients with AB but only slightly elevated in those with CPE. To interpret these data we used an electromechanical analogue including serial inhomogeneity with shunt impedance. From this model we concluded that AB causes both the central and peripheral airway resistances to increase, while CPE brings about a rise mainly in peripheral resistance. In IP patients, only the imaginary part of Zt decreased, which might reflect the decrease in both lung and chest wall compliance. In CPE patients, but not in AB patients, the real part of Zt fell. These data were consistent with the assumption that the decrease in mass per unit volume of lung tissue and hyperinflation of the chest wall in CPE patients might lower the tissue resistances.
The effects of an antimuscarinic agent, oxitropium bromide (200 micrograms), a beta-2 adrenoceptor agonist, fenoterol (200 micrograms), and their combination, were compared in ten patients with chronic obstructive pulmonary disease and ten patients with bronchial asthma, in a placebo-controlled, single blind crossover trial. In patients with chronic obstructive pulmonary disease, oxitropium and fenoterol produced a significant and similar degree of bronchodilatation. The duration of the bronchodilator effect was 3 h after oxitropium and 4 h after fenoterol, respectively. The combination of oxitropium and fenoterol produced a significantly greater degree of bronchodilatation than either drug alone. The duration of bronchodilatation in combination was 7 h and was considerably longer than that of each drug alone. In patients with bronchial asthma, oxitropium and fenoterol also caused bronchodilatation. Their combination produced a significantly greater degree of bronchodilatation than when either drug was used. The duration of the bronchodilator effects were 5 h after oxitropium, 4 h after fenoterol and 5 h after the combination. We conclude that the combination of oxitropium and fenoterol causes greater bronchodilatation in patients with chronic obstructive pulmonary disease and bronchial asthma than when compared to each drug alone. In the former, the duration of bronchodilatation is additionally prolonged. These combination effects may be of value in the clinical management of these common respiratory disorders.
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