Abstract

Magnesium sulfate has been shown to have a bronchodilating effect in asthma, but this effect has not been clearly established in the context of chronic obstructive pulmonary disease (COPD). For this reason we investigated the possible bronchodilating effect of magnesium sulfate in COPD exacerbations. We studied 24 patients with exacerbated COPD who required admission to our hospital's pneumology department. All patients underwent baseline spirometry and were subsequently randomized to groups in a double-blind crossover design. Patients received 1.5 g of magnesium sulfate or placebo in an intravenous solution for 20 minutes. Those who received magnesium sulfate the first day were given placebo the second day, and vice versa. Spirometry was performed 15, 30, and 45 minutes after administration of magnesium sulfate or placebo. Finally, 400 microg of salbutamol were administered using a spacer and a final spirometry was performed 15 minutes later. All patients also received treatment with corticosteroids, intravenous antibiotics, oxygen, and regularly-scheduled bronchodilator therapy (salbutamol and ipratropium bromide every 6 hours). When we compared absolute increase in milliliters and percentage increase in forced expiratory volume in 1 second (FEV1) obtained with magnesium sulfate application to the increases obtained with placebo after 15, 30, and 45 minutes, no significant differences were found. When we compared absolute and percentage increases in FEV1 after administering salbutamol, we found significantly greater increases after magnesium sulfate administration. The mean (SD) absolute increase in FEV1 was 0.18 [corrected] (0.42) L after magnesium sulfate administration and 0.081 [0.01] L after placebo (P=.004). The percentage increase in FEV1 was 17.11% (3.7%) after magnesium sulfate and 7.06% (1.8%) after placebo (P=.008). Intravenous administration of magnesium sulfate has no bronchodilating effect in patients with COPD exacerbations. It does, however, enhance the bronchodilating effect of inhaled ss2-agonists.

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