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Worsening of underlying bronchospasm may be associated with acute exacerbations of chronic obstructive pulmonary disease (COPD). As airway obstruction becomes more severe, the therapeutic option is to add a short-acting inhaled beta2-agonist as needed to cause rapid relief of bronchospasm. Unfortunately however, the most effective dosage may increase above that recommended during acute exacerbations. Formoterol (Oxis) Turbuhaler has a rapid onset of action (within minutes) and demonstrates a maintained effect on a rway function. In this study, we examined the effects of formoterol used as needed in 20 patients with acute exacerbations of COPD. A dose response curve to inhaled formoterol (9 microg per inhalation) or placebo was constructed using three separate inhalations, i.e. a total cumulative dose of 27 microg. Dose increments were given at 20-min intervals, with measurements being made 15 min after each dose. Formoterol, but not placebo, induced a large and significant (P<0.001) dose-dependent increase in forced expiratory volume in 1 sec (FEV1) [mean differences from baseline = 0.1311 after 9 microg formoterol (95% CI: 0.096-0.167)] 0.1811 after 18 microg formoterol (95% CI: 0.140-0.2221) and 0.2081 after 27 microg formoterol (95% CI: 0.153-0.2631). However, 27 microg formoterol did not induce further benefit [0.0271 (95% CI: -0.008-0.0621); P=0.121] when compared wth 18 microg formoterol. Results of this study suggest the use of higher than customary dose of formoterol for as-needed therapy to provide rapid relief of bronchospasm in patients suffering from acute exacerbations of partially reversible COPD.

We examined whether a pretreatment with formoterol, oxitropium bromide, or salmeterol might modify the dose-response curves to inhaled salbutamol in patients with stable and partially reversible chronic obstructive pulmonary disease (COPD). Sixteen outpatients with partially reversible, stable COPD received 24 microg formoterol, 50 microg salmeterol, 200 microg oxitropium bromide, or placebo on four non-consecutive days. Spirometric testing was performed immediately before inhalation of treatment and after 2 h. A dose-response curve to inhaled salbutamol was then constructed using doses of 100, 100, 200 microg and 400 microg--that is, a total cumulative dose of 800 microg. Dose increments were given at 20 min intervals with measurements being made 15 min after each dose. Formoterol, salmeterol, or oxitropium bromide elicited a significant increase in forced expiratory volume in one second (FEV1) compared with placebo (mean differences (L) = placebo 0.05; formoterol 0.34; salmeterol 0.27; oxitropium bromide 0.23). Dose-dependent increases in FEV1 were seen (mean values (L) before salbutamol and after a cumulative dose of 100, 200, 400, and 800 microg = placebo: 1.06, 1.28, 1.35, 1.39, 1.41; formoterol: 1.33, 1.37, 1.41, 1.44, 1.44; salmeterol: 1.30, 1.33, 1.36, 1.39, 1.42; oxitropium bromide: 1.27, 1.34, 1.37, 1.41, 1.40). Statistical analysis revealed no significant differences in FEV1 and forced vital capacity (FVC) responses to salbutamol after therapy with formoterol, salmeterol, or oxitropium bromide compared with placebo. This study clearly shows that a pretreatment with a conventional dose of formoterol, salmeterol, or oxitropium bromide does not preclude the possibility of inducing a further bronchodilation with salbutamol in patients suffering from partially reversible chronic obstructive pulmonary disease.

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The assessment of reversibility is recognized as being an essential part of the management of airways obstruction, but testing for reversibility of airways obstruction may not be useful for identifying patients with chronic obstructive pulmonary disease (COPD) who are likely to benefit from bronchodilator treatment. We studied 100 patients with stable COPD. Early reversibility of airways obstruction to 200 mg salbutamol and peak bronchodilation to 50 micrograms salmeterol or 200 micrograms salbutamol were evaluated in four different sessions (two for salbutamol and two for salmeterol), using a double-blind, cross-over, randomized study. Fifteen minutes after inhalation of salbutamol, 47 patients presented an increase in FEV1 greater than 15% of baseline, whereas 48 showed an increase of FEV1 of at least 160 ml from basal value and 33 an increase in FEV1 greater than both 15% of baseline and 200 ml. On the contrary, 69 patients presented an increase in FEV1 greater than 15% of baseline, 65 an increase of FEV1 of at least 160 ml from basal value and 60 an increase in FEV1 greater than both 15% of baseline and 200 ml as maximum increase over baseline usually 2-4 h after inhalation of salmeterol. Twenty-seven other subjects defined as irreversible by the lack of acute improvement in FEV1 after salbutamol, showed an increase in FEV1 greater than 15% of baseline, 20 showed an increase of FEV1 of at least 160 ml from basal value, and 18 showed an increase in FEV1 greater than both 15% of baseline and 200 ml; all had the maximum degree of bronchodilation usually 1-2 h after salbutamol administration. These findings clearly demonstrate that many patients suffering from stable COPD show early reversibility to a short-acting beta 2-agonist and patients who do not manifest early reversibility to salbutamol can still benefit from salbutamol or salmeterol. Therefore, treatments with beta 2-agonists must always be tried.