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Acute tetrahydrobiopterin restores endothelial function in patients with COPD (1123.1)
Author(s) -
Harris Ryan,
Seigler Nichole,
Halasan Karen,
Livieratos Speros,
Dillard Thomas,
Bass Leon
Publication year - 2014
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.28.1_supplement.1123.1
Subject(s) - tetrahydrobiopterin , medicine , copd , nitric oxide , enos , endothelial dysfunction , placebo , ingestion , bioavailability , gastroenterology , endocrinology , nitric oxide synthase , pharmacology , pathology , alternative medicine
Chronic obstructive pulmonary disease (COPD), although a disease of the lungs, is accompanied by systemic oxidative stress and inflammation, both of which contribute to reductions in nitric oxide (NO) bioavailability. Tetrahydrobiopterin (BH4) is an essential cofactor for eNOS and subsequent NO bioavailability. This study sought to determine if acute ingestion of BH4 improves endothelial function in patients with COPD. 18 patients with COPD and 15 healthy controls participated in this study. The flow‐mediated dilation (FMD) test was performed at baseline in all subjects, and 3 hours following ingestion of either BH4 (5 mg/kg of Kuvan®) dissolved in 4oz of apple juice or placebo only in patients. No differences in sex or race were observed between groups. Age (56±2 vs. 57±2 yrs.), BMI (31.5±1.9 vs. 26.6±1.6 kg/m2), and MAP (93.9±2.8 vs. 88.0±2.7 mm Hg) were all similar (p>0.05) between patients and controls, respectively. FEV1 was significantly lower in patients (56±4 vs. 103±4 %predicted) compared to controls. At baseline, FMD was lower (p=0.046) in patients (4.9±0.5%) compared to controls (6.9±0.9%). Acute BH4 treatment significantly improved FMD (α3.4±0.6%; p<0.001) in patients; however, no change (α‐0.2±0.6%; p=0.703) in FMD was observed following placebo. Findings from this study demonstrate that a single dose of BH4 transiently restores endothelial function in patients with COPD to the values observed in controls. Supported by the American Heart Association (RAH). Grant Funding Source : Supported by AHA 10SDG305006 (RAH)