Nebulized glyceryl trinitrate exerts acute bronchodilator effects in patients with acute bronchial asthma

Glyceryl trinitrate (GTN) is a potent smooth muscle relaxant and vasodilator. There are conflicting reports regarding its efficacy as a bronchodilator. The aim of this study was to examine whether nebulized GTN has bronchodilating effects in patients with acute bronchial asthma. We studied 18 patients (five female, 13 male) who were admitted to the hospital with acute severe asthma on two occasions, administering either 6 mg nebulized GTN or placebo (saline) in a double-blind, randomized, crossover fashion. Bronchial response was assessed by measurement of peak expiratory flow (PEF), forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC). A systematic effect of this dose of GTN was demonstrated by a mean increase in heart rate of 38.1% (SEM=7.6%) after GTN administration from supine to erect posture, compared with 10.2% (SEM=1.8%) after placebo (P<0.005). Systolic blood pressure decreased by 8.7% (SEM=1.1%) after GTN, compared with 4.0% (SEM=2.1%) after placebo (P<0.05). Diastolic blood pressure did not change significantly. Baseline PEF, FEV1 and FVC did not differ on the two experimental days; however, acute bronchodilating effects were seen: PEF (l/min); 368 (21) pre-GTN, 411 (22) post-GTN and 384 (23) post-placebo (P<0.001). FEV1 (l); 2.12 (0.13) pre-GTN, 2.46 (0.15) post-GTN and 2.25 (0.16) post-placebo (P<0.001). FVC (l); 3.31 (0.17) pre-GTN, 3.75 (0.2) post-GTN and 3.54 (0.2) post-placebo (P<0.001). In conclusions, nebulized GTN has bronchodilating effects in patients with acute bronchial asthma. The exact mechanism of bronchodilation is not known, but it may be due to local effect on bronchial smooth muscles through nitric oxide or by systemic vasodilatation which leads to a decrease in pulmonary artery pressure and pulmonary vascular resistance, or an increase in systemic catecholamine release.