Blunted vascular response to pulmonary rehabilitation in COPD patients and impaired exercise-induced mobilization of endothelial-colony forming cells

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Desplanche, Elodie | Blervaque, Léo | Günther, Sven | Gruest, Maxime | Philippe, Aurélien | Rancic, Jeanne | Gendron, Nicolas | Hédon, Christophe | Perez-Martin, Antonia | Virsolvy, Anne | Cazorla, Olivier | Dauvilliers, Yves | Hayot, Maurice | Bourdin, Arnaud | Rossi, Elisa | Smadja, David M | Gouzi, Fares

Edité par CCSD ; European Respiratory Society -

International audience. Introduction: Cardiovascular comorbidities in Chronic Obstructive Pulmonary Disease (COPD) have been related to an endothelial dysfunction, which was not responsive to exercice training. Endothelial Colony-Forming Cells (ECFCs) are vasculogenic endothelial progenitor cells that can be mobilized in response to different stimuli. Thus, we aimed to compare the mobilization of ECFCs in healthy control subjects (HC) and COPD patients in response to an acute maximal exercise.Methods: Reactive Hyperhemia Index (RHI) during post-occlusive pulse-arterial tonometry (EndoPAT®), maximal blood pressure (BP) and V’O2max assessments during a maximal test were performed before and after 4-6 weeks of training in 20 HC (60.91 ± 1.7 y.o, 11 females) and 19 COPD (61.1 ± 1.9 y.o, 9 females) patients. Blood Mononuclear cells (Mo) were collected before and 30min after the exercise and cultured to isolate ECFC colonies. Group (G), Time (T) and Group*Time interaction (G*T) effects were tested with mixed linear models.Results: Training did not improve maximal systolic BP (G*T: p<0.05) and RHI in patients COPD (G: p<0.01). Before training, the acute maximal exercise mobilized ECFCs colonies in HC only (+0.59±0.93 vs. +0.05±0.47/107 Mo; G: p=0.71; T: p<0.001; G*T: p<0.05). This ECFCs mobilization was significantly correlated with markers of vascular function in HC (RHI: r=0.39, p<0.05; V’O2max: r=0.48, p<0.01; max systolic BP: r=0.47; p<0.05).Conclusion: The physiological mobilization of vascular endothelial progenitor cells in response to an acute exercise was blunted in COPD patients and could explain the impaired vascular response to training.

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