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Cardiovascular Research 1999 43(1):228-236; doi:10.1016/S0008-6363(99)00059-0
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Adenosine plasma concentration in pulmonary hypertension

Alain Y. Saadjiana,d,*, Franck Paganellia, Martine L. Reynaud Gaubertb, Samuel Levya and Régis P. Guieuc

aCardiology Department, C.H.U Nord, 13915 Marseille cedex 20, France
bPneumology Department, C.H.U Nord, 13915 Marseille cedex 20, France
cCentre National de la Recherche Scientifique: UMR 6560 and Biochemistry Department, C.H.U Nord, 13915 Marseille cedex 20, France
dInstitut National de la Santé et de la Recherche Médicale, C.H.U Nord, 13915 Marseille cedex 20, France

* Corresponding author. Tel.: +33-04-9196-8684; fax: +33-04-9196-2162

Objective: In this study, we sought to appreciate the role of adenosine in the regulation of pulmonary vascular tone, especially in the case of clinical pulmonary hypertension, by investigating the relationship between endogenous plasma adenosine levels and pulmonary artery vasoconstriction. Methods: Adenosine plasma concentrations, were measured simultaneously in the distal right pulmonary artery and in the femoral artery, both at steady state (room air) and during pure oxygen inhalation. Three clinical situations were considered: (1) normal hemodynamics [7 control subjects, mean pulmonary artery pressure (MPAP)=18.5±1 mm Hg], (2) moderate pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD), (8 patients, MPAP=31±3 mm Hg), (3) severe primary pulmonary hypertension (PPH), (8 patients, MPAP=70±5 mm Hg). Results: In every instance, adenosine evaluated by HPLC was higher in the pulmonary than in the systemic circulation. For room air, adenosine plasma concentrations were significantly lower in COPD (0.49±0.16 µmol l–1) and PPH patients (0.45±0.14 µmol l–1) than in controls (1.26±0.12 µmol l–1). During O2 administration, adenosine plasma concentrations all decreased but more so in COPD and PPH patients. The significant correlations between adenosine plasma concentrations and both pulmonary vascular resistance and PvO2, in controls, were not found in COPD or PPH patients. Conclusion: The adenosine plasma concentrations in the pulmonary circulation of PPH and COPD patients are low, and may contribute to pulmonary artery hypertension.

KEYWORDS Adenosine; Pulmonary circulation; Hemodynamics; Hypoxia/anoxia; Endothelial function


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