Plasma beta-endorphin and adenosine concentration in pulmonary hypertension

To determine whether β-endorphin plays a role in the regulation of pulmonary vascular tone in patients with pulmonary hypertension, we investigated the relations between hemodynamics and β-endorphin and adenosine concentrations in 3 clinical situations: (1) normal hemodynamics (7 subjects, mean pulm...

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Bibliographic Details
Published in:	The American journal of cardiology Vol. 85; no. 7; pp. 858 - 863
Main Authors:	Saadjian, Alain Yves, Paganelli, Franck, Juin, Maria-Annick, Devaux, Christiane, Lévy, Samuel, Guieu, Régis Pierre
Format:	Journal Article
Language:	English
Published:	New York, NY Elsevier Inc 01-04-2000 Elsevier Elsevier Limited
Subjects:	Adenosine - blood Adult beta-Endorphin - blood Biological and medical sciences Biomarkers - blood Blood Gas Analysis Cardiology Female Hormones Humans Hypertension Hypertension, Pulmonary - blood Hypertension, Pulmonary - etiology Hypertension, Pulmonary - physiopathology Hypertension, Pulmonary - therapy Lung Diseases, Obstructive - blood Lung Diseases, Obstructive - complications Lung Diseases, Obstructive - physiopathology Lung Diseases, Obstructive - therapy Male Medical sciences Middle Aged Oxygen Inhalation Therapy Pneumology Prognosis Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases Pulmonary Wedge Pressure Radioimmunoassay Human Lung disease Adenosine Purine nucleoside Pathophysiology Respiratory disease Idiopathic Cardiovascular disease Exploration β-Endorphin Pulmonary hypertension Bronchus disease Complication Obstructive pulmonary disease Hemodynamics Comparative study
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Summary:	To determine whether β-endorphin plays a role in the regulation of pulmonary vascular tone in patients with pulmonary hypertension, we investigated the relations between hemodynamics and β-endorphin and adenosine concentrations in 3 clinical situations: (1) normal hemodynamics (7 subjects, mean pulmonary artery [PA] pressure 18.5 ± 1 mm Hg); (2) moderate pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD) (8 patients, mean PA pressure 31 ± 3 mm Hg); and (3) severe primary pulmonary hypertension (PPH) (8 patients, mean PA pressure 70 ± 5 mm Hg). Plasma β-endorphin and adenosine were measured in a distal PA and in the femoral artery in room air and during oxygen inhalation. Beta-endorphin levels were similar in the pulmonary and systemic circulations. No difference was observed between patients with COPD and PPH, but relative to controls, both had significantly higher β-endorphin levels. Pulmonary adenosine was significantly lower in patients with pulmonary hypertension than in controls (−60% in COPD [p <0.005] and −70% in PPH [p <0.001]). Pure oxygen administration significantly decreased adenosine and β-endorphin levels, much more so in patients with COPD and PPH. We found a negative correlation between β-endorphin and adenosine concentrations (r = −0.751, p <0.001): the higher the adenosine, the lower the β-endorphin level. These observations suggest that because adenosine release by pulmonary vascular endothelium is reduced in pulmonary hypertension, the resulting worsened hypoperfusion and tissue oxygenation may cause increased β-endorphin release.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0002-9149 1879-1913
DOI:	10.1016/S0002-9149(99)00881-4