COMPARISON OF THE EFFECTS OF ADENOSINE AND NIFEDIPINE IN PULMONARY-HYPERTENSION

The hemodynamic effects of intravenously administered adenosine, a pot ent vasodilator, were examined in 15 patients with pulmonary hypertens ion. All patients were given adenosine, 50-mu-g/kg per min, increased by 50-mu-g/kg per min at 2 min intervals to a maximum of 500-mu-g/kg p er min or until the development of untoward side effects. The patients were then given oral nifedipine, 20 mg every hour, until a greater-th an-or-equal-to 20% decrease in pulmonary vascular resistance or system ic hypotension occurred. The administration of maximal doses of adenos ine, 256 +/- 46-mu-g/kg per min, produced a 2.4% reduction in pulmonar y artery pressure (p = NS), a 37% decrease in pulmonary vascular resis tance (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) an d an 8% increase in cardiac index (p = NS). There was a significant co rrelation (r = 0.714, p = 0.01) between the reduction in pulmonary vas cular resistance that resulted from adenosine administration and that achieved with the administration of nifedipine. Six patients had subst antial reductions in pulmonary vascular resistance with adenosine but not with nifedipine. Thus, adenosine is an effective vasodilator in pa tients with pulmonary hypertension and can be used for safe and rapid assessment of vasodilator reserve in these patients. The ability of ad enosine to reduce pulmonary vascular resistance by 37%, and its effect iveness in patients in whom nifedipine was not, suggests that the purs uit of an oral analogue of adenosine as a therapeutic agent is warrant ed.