Plasma beta-endorphin and adenosine concentration in pulmonary hypertension

To determine whether beta-endorphin plays a role in the regulation of pulmo nary vascular tone in patients with pulmonary hypertension, we investigated the relations between hemodynamics and beta-endorphin and adenosine concen trations in 3 clinical situations: (1) normal hemodynamics (7 subjects, mea n pulmonary artery [PA] pressure 18.5 +/- 1 mm Hg); (2) moderate pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD) (8 p atients, mean PA pressure 31 +/- 3 mm Hg); and (3) severe primary pulmonary hypertension (PPH) (8 patients, mean PA pressure 70 +/- 5 mm Hg), Plasma b eta-endorphin and adenosine were measured in a distal PA and in the femoral artery in room air and during oxygen inhalation. Beta-endorphin levels wer e similar in the pulmonary and systemic circulations. No difference was obs erved between patients with COPD and PPH, but relative to controls, both ha d significantly higher beta-endorphin levels. Pulmonary adenosine was signi ficantly lower in patients with pulmonary hypertension than in controls (-6 0% in COPD [p <0.005] and -70% in PPH [p <0.001]). Pure oxygen administrati on significantly decreased adenosine and beta-endorphin levels, much more s o in patients with COPD and PPH. We found a negative correlation between p- endorphin and adenosine concentrations (r = -0.751, p < 0.001): the higher the adenosine, the lower the beta-endorphin level. These observations sugge st that because adenosine release by pulmonary vascular endothelium is redu ced in pulmonary hypertension, the resulting worsened hypoperfusion and tis sue oxygenation may cause increased beta-endorphin release. (C)2000 by Exce rpta Medico, Inc.