Document Detail


Role of oxidative stress in remodeling of the myocardial microcirculation in hypertension.
MedLine Citation:
PMID:  16709946     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: We tested the hypothesis that in early hypertension (HT), increased oxidative stress leads to myocardial microvascular remodeling. METHODS AND RESULTS: Pigs were studied after a 12-week observation: normal (n=8), untreated renovascular HT (n=8), or HT+chronic antioxidant supplementation (HT+A, n=6). Left ventricular muscle mass (LVMM) and myocardial blood flow (MBF) reserve were determined using electron beam computer tomography (CT), and the spatial density and tortuousity of myocardial microvessels (<500 microm) was then measured in myocardial samples with micro-CT. Myocardial microvascular morphology, oxidative stress, inflammation, and growth factor expression were determined in vitro. HT and HT+A had similarly increased arterial pressure and LVMM, but only HT showed impaired MBF response to adenosine. Compared with normal, HT had increased spatial density of myocardial microvessels, which was preserved in HT+A (111.8+/-7.8, 166.3+/-15.7, and 106.4+/-6.1 vessels per cm2, respectively). HT also showed microvascular wall thickening, increased systemic and tissue oxidative stress, inflammation, and expression of vascular endothelial growth factor and its receptor Flk-1, most of which were attenuated by antioxidants. CONCLUSIONS: Myocardial microvascular remodeling in early HT is accompanied by tissue oxidative stress, inflammation, and altered growth factor expression, and attenuated by antioxidant intervention. This study underscores a role of increased oxidative stress in modulating myocardial microvascular architecture in early HT.
Authors:
Xiang-Yang Zhu; Elena Daghini; Alejandro R Chade; Martin Rodriguez-Porcel; Claudio Napoli; Amir Lerman; Lilach O Lerman
Related Documents :
11930186 - Echocardiographic and magnetic resonance methods for diagnosing hibernating myocardium.
10637086 - Prediction of global left ventricular function after bypass surgery in patients with se...
22221696 - The chinese version of the myocardial infarction dimensional assessment scale (midas): ...
10946026 - Comparison of low-dose dobutamine ventriculography with low-dose dobutamine echocardiog...
6609236 - Circulating immune complexes containing igg, iga and igm in patients with myocardial in...
11488406 - Lecithinized copper, zinc-superoxide dismutase ameliorates ischemia-induced myocardial ...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-05-18
Journal Detail:
Title:  Arteriosclerosis, thrombosis, and vascular biology     Volume:  26     ISSN:  1524-4636     ISO Abbreviation:  Arterioscler. Thromb. Vasc. Biol.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-07-21     Completed Date:  2006-08-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9505803     Medline TA:  Arterioscler Thromb Vasc Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1746-52     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / administration & dosage,  pharmacology
Blood Vessels / physiopathology
Coronary Circulation*
Drug Administration Schedule
Female
Hypertension, Renovascular / complications,  pathology,  physiopathology*
Microcirculation
Myocarditis / etiology,  pathology
Myocardium / metabolism*,  pathology
Oxidative Stress* / drug effects
Swine
Tomography, X-Ray Computed
Grant Support
ID/Acronym/Agency:
EB00305/EB/NIBIB NIH HHS; HL-63282/HL/NHLBI NIH HHS; HL77131/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants

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


Previous Document:  Laminar shear stress inhibits cathepsin L activity in endothelial cells.
Next Document:  Activation of alveolar macrophages via the alternative pathway in herpesvirus-induced lung fibrosis.