Effect of salbutamol on respiratory muscle function and ventilation in awake canines

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The effect of the beta-agonist bronchodilator salbutamol on respiratory muscles and ventilation is uncertain. The presence of beta2 receptors on skeletal muscles and increased diaphragm contractility in vitro with salbutamol predict a significant effect that has not been confirmed, in vivo in non-fatigued diaphragm or in clinical studies using standard bronchodilator dosages. Therefore, we infused salbutamol at a higher dosage (23.3 microg/min) used clinically for treatment of respiratory emergencies, while measuring directly the length, shortening and EMG activation of costal and crural diaphragm, parasternal intercostal and transversus abdominis muscles, in 10 awake canines. At this salbutamol dosage, ventilation and tidal volume increased significantly during both resting and CO2-stimulated breathing. Salbutamol elicited significant increases in respiratory muscle shortening with much smaller increases in EMG activity, so the proportionally greater muscle shortening per unit EMG showed increased muscle contractility. The effects of salbutamol were not extinguished by inspiratory flow resistance or fluid challenge but were reversed specifically by the beta-blocker, propranolol. This study demonstrates that, in sufficient intravenous dosage, the beta-agonist salbutamol elicits increased ventilation and a beta2 receptor-mediated increase in contractility of respiratory muscles.