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Vascular Dysfunction in Chronic Obstructive Pulmonary Disease (COPD): The Role of Mitochondrial‐derived Oxidative Stress
Author(s) -
Kwon Oh Sung,
Layec Gwenael,
Broxterman Ryan M,
Gifford Jayson R,
Park Soung Hun,
Shields Katherine L,
Richardson Russell S
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.527.10
Subject(s) - medicine , oxidative stress , copd , area under the curve , vasodilation , cardiology , endothelial dysfunction , population , environmental health
Background This study sought to determine the contribution of mitochondrial‐derived oxidative stress in the vascular dysfunction exhibited by patients with COPD. Methods Vascular function was assessed with brachial artery flow‐mediated vasodilation (FMD) and the hyperemic response to both single and continuous passive leg movement (PLM) in 10 patients with COPD (55–70 years) before and after both the acute and chronic ingestion (4 weeks) of a mitochondrial‐targeted antioxidant (MitoQ) (20mg/day). Results Baseline % FMD (2.5 ± 0.9 %) in the patients with COPD was significantly enhanced by both the acute (3.3 ± 0.8 %) and 4 week (5.3 ± 1.2 %) MitoQ consumption. Acute MitoQ had no effect on the single PLM‐induced change in peak LBF (ΔPeak) or the area under the leg blood flow (LBF) response curve (AUC), but the 4 week MitoQ consumption significantly augmented both the single PLM ΔPeak (190±184 vs. 300±96 ml/min) and LBF AUC (20±14 vs. 50±16 ml). Compared to baseline (ΔPeak = 300±84 ml/min; LBF AUC = 80±34 ml), both ΔPeak and LBF AUC during continuous PLM‐were significantly enhanced with both the acute (ΔPeak: 435±96 ml/min; LBF AUC: 105±56 ml) and 4 week (ΔPeak: 622±106 ml/min; LBF AUC: 300±120 ml) MitoQ consumption. Conclusions This study reveals that, in patients with COPD, mitochondrial‐derived oxidative stress contributes significantly to the vascular dysfunction exhibited by this population. Therefore, targeting mitochondrial‐derived oxidative stress may, through an improvement in vascular function, be an efficacious approach to combat cardiovascular disease in patients with COPD. Support or Funding Information This work was funded, in part, by the National Heart, Lung, and Blood Institute at the National Institute of Health (PO1 HL1091830, K99HL 125756 and T32 HL139451), the Flight Attendant Medical Research Institute (FAMRI), and the Veteran's Administration Rehabilitation Research and Development Service (E6910‐R, E1697‐R, E1433‐P, E9275‐L and E1572‐P). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .