Document Detail

NO and EDHF Pathways in Pulmonary Arteries and Veins are Impaired in COPD Patients.
MedLine Citation:
PMID:  22609132     Owner:  NLM     Status:  Publisher    
We investigated endothelial function of both pulmonary arteries and veins in patients with chronic obstructive pulmonary disease (COPD) of varying severity in regard to the role of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Lung tissues were obtained from patients undergoing lobectomy or pneumonectomy. Patients were grouped to control, moderate COPD, and severe COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. Pulmonary arteries and veins were studied for endothelium-dependent relaxations. NO concentration was measured by electrochemical method. Protein expressions of eNOS and phosphorylated eNOS were determined by Western-blot. Endothelium-dependent relaxation was more significant in pulmonary arteries than in veins. The vasorelaxation was decreased in patients of moderate COPD and further decreased in severe COPD. The severity of endothelial dysfunction in both pulmonary arteries and veins correlated with the degree of airflow obstruction. COPD patients exhibited reduced endothelial NO production, decreased eNOS protein expression and decreased eNOS phosphorylation. The EDHF component was abolished in the pulmonary vasculature of patients with severe COPD. NO and EDHF pathways are both involved in the regulation of vascular tone in human pulmonary arteries and veins. Both pathways are impaired in COPD patients and the severity of the impairment increases with the progress of the disease. Downregulation of eNOS expression and inhibition of eNOS activation underlie the reduction of NO in COPD patients.
Qin Yang; Norihisa Shigemura; Malcolm John Underwood; Michael Hsin; Hong-Mei Xue; Yu Huang; Guo-Wei He; Cheuk-Man Yu
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-5-15
Journal Detail:
Title:  Vascular pharmacology     Volume:  -     ISSN:  1879-3649     ISO Abbreviation:  -     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-5-21     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101130615     Medline TA:  Vascul Pharmacol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012. Published by Elsevier Inc.
Division of Cardiology, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong & TEDA International Cardiovascular Hospital, Medical College, Nankai University, Tianjin, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  From excess adiposity to insulin resistance: The role of free fatty acids.
Next Document:  The Emerging Challenge in Diabetes: The "Metabolic Memory"