Comparison of the effects of adenosine and nifedipine in pulmonary hypertension

The hemodynamic effects of intravenously administered adenosine, a potent vasodilator, were examined in 15 patients with pulmonary hypertension. All patients were given adenosine, 50 μg/kg per min, increased by 50 μg/kg per min at 2 min intervals to a maximum of 500 μg/kg per min or until the development of untoward side effects. The patients were then given oral nifedipine, 20 mg every hour, until a ≥20% decrease in pulmonary vascular resistance or systemic hypotension occurred. The administration of maximal doses of adenosine, 256 ± 46 μg/kg per min, produced a 2.4% reduction in pulmonary artery pressure (p = NS), a 37% decrease in pulmonary vascular resistance (p < 0.001) and a 57% increase in cardiac index (p < 0.001). The administration of maximally effective doses of nifedipine (91 ± 36 mg) produced a 15% reduction in the mean pulmonary artery pressure (p < 0.05), a 24% decrease in pulmonary vascular resistance (p < 0.01) and an 8% increase in cardiac index (p = NS). There was a significant correlation (r = 0.714, p = 0.01) between the reduction in pulmonary vascular resistance that resulted from adenosine administration and that achieved with the administration of nifedipine. Six patients had substantial reductions in pulmonary vascular resistance with adenosine but not with nifedipine. Thus, adenosine is an effective vasodilator in patients with pulmonary hypertension and can be used for safe and rapid assessment of vasodilator reserve in these patients. The ability of adenosine to reduce pulmonary vascular resistance by 37%, and its effectiveness in patients in whom nifedipine was not, suggests that the pursuit of an oral analogue of adenosine as a therapeutic agent is warranted.