Vasodilators have been a main focus of therapy for primary pulmonary h
ypertension, Adenosine and prostacyclin have been shown to reduce pulm
onary vascular resistance acutely in these patients, In order to compa
re the acute hemodynamic effects of adenosine and prostacyclin, ten pa
tients with severe primary pulmonary hypertension, unresponsive to med
ical therapy, were studied, After baseline hemodynamics were obtained,
an adenosine infusion, 50 to 100 ng/kg/min, was begun and titrated to
the maximum tolerated dose, Hemodynamics were allowed to return to ba
seline, and thereafter, a prostacyclin infusion was begun at 2 ng/kg/m
in, and titrated to the maximum tolerated dose, Overall, adenosine (20
0 +/- 53 ng/kg/min) produced a 33 +/- 18% (p<0.001) fall in pulmonary
vascular resistance and a 52 +/- 25% (p<0.001) increase in cardiac out
put with no effect on pulmonary or systemic arterial pressures. Prosta
cyclin (8 +/- 4 ng/kg/min) caused a 22 +/- 18% (p<0.01) fall in pulmon
ary vascular resistance and a 25 +/- 26% (p<0.05) increase in cardiac
output with a 14 +/- 6% (p<0.001) decrease in systemic arterial pressu
re, but no change in pulmonary arterial pressure, The effects of adeno
sine and prostacyclin on pulmonary vascular resistance were similar (r
=0.70, r(2)=0.49, p=0.02). Adenosine and prostacyclin have similar hem
odynamic effects acutely in primary pulmonary hypertension, Adenosine
may be useful as a test of the potential for long-term prostacyclin th
erapy in patients with primary pulmonary hypertension,