The Effect of Six Months of Daily Treatment with the Beta-2 Agonist Oral Pirbuterol on Pulmonary Hemodynamics in Patients with Chronic Hypoxic Cor Pulmonale Receiving Long-term Oxygen Therapy

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Abstract
We studied the acute and long-term effect of the oral beta-2 agonist pirbuterol on pulmonary hemodynamics and right and left ventricular ejection fractions in 11 patients with stable hypoxic chronic bronchitis and emphysema who were maintained on long-term oxygen therapy. We have used a double-blind study with random allocation of patients to receive either pirbuterol or an identical-appearing placebo. Six patients received 15 mg pirbuterol thrice daily, and five patients received a similar placebo thrice daily, over a 6-month period. The first 15-mg dose of pirbuterol by mouth at the beginning of the study raised the heart rate from 84 .+-. 13 to 100 .+-. 16 beats/min (mean .+-. SD) (p < 0.01), and cardiac output from 5.2 .+-. 0.9 to 6.4 .+-. 0.8 L/min (p < 0.01) and right ventricular ejection fraction (RVEF) from 0.28 .+-. 0.10 to 0.33 .+-. 0.12 (p < 0.01) within 120 min after receiving the drug, but without significant change in the mean pulmonary arterial pressure. None of these variables changed significantly after an acute dose of placebo in another four patients. Repeated measurements after 6 months of chronic oral therapy with either pirbuterol or placebo showed that 16 h after the last 15-mg oral dose of pirbuterol or placebo, the heart rate, mean pulmonary arterial pressure, cardiac output, total pulmonary vascular resistance, and RVEF were all not significantly different from the values 6 months previously, before receiving either pirbuterol or the placebo. Furthermore, after 6 months of chronic oral therapy with pirbuterol, one further single 15-mg dose by mouth no longer produced significant changes in either cardiac output or RVEF. We conclude that the beta-2 agonist pirbuterol increased cardiac output, without further rise in pulmonary arterial pressure, when given acutely to patients with chronic hypoxic cor pulmonale who were receiving long-term oxygen therapy. However, the drug appeared to lose these hemodynamic effects during 6 months of chronic oral therapy.