Document Detail


Microvascular function in younger adults with obesity and metabolic syndrome: role of oxidative stress.
MedLine Citation:
PMID:  23934859     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Older adults with cardiovascular disease exhibit microvascular dysfunction and increased levels of reactive oxygen species (ROS). We hypothesized that microvascular impairments begin early in the disease process and can be improved by scavenging ROS. Forearm blood flow (Doppler ultrasound) was measured in 45 young (32 ± 2 yr old) adults (n = 15/group) classified as lean, obese, and metabolic syndrome (MetSyn). Vasodilation in response to endothelial (ACh) and vascular smooth muscle [nitroprusside (NTP) and epoprostenol (Epo)] agonists was tested before and after intra-arterial infusion of ascorbic acid to scavenge ROS. Vasodilation was assessed as a rise in relative vascular conductance (ml·min(-1)·dl(-1)·100 mmHg(-1)). ACh and NTP responses were preserved (P = 0.825 and P = 0.924, respectively), whereas Epo responses were lower in obese and MetSyn adults (P < 0.05) than in lean controls. Scavenging of ROS via infusion of ascorbic acid resulted in an increase in ACh-mediated (P < 0.001) and NTP-mediated (P < 0.001) relative vascular conductance across all groups, suggesting that oxidative stress influences vascular responsiveness in adults with and without overt cardiovascular disease risk. Ascorbic acid had no effect on Epo-mediated vasodilation (P = 0.267). These results suggest that obese and MetSyn adults exhibit preserved endothelium-dependent vasodilation with reduced dependence on prostacyclin and are consistent with an upregulation of compensatory vascular control mechanisms.
Authors:
Jacqueline K Limberg; John W Harrell; Rebecca E Johansson; Marlowe W Eldridge; Lester T Proctor; Joshua J Sebranek; William G Schrage
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-08-09
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  305     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2013 Oct 
Date Detail:
Created Date:  2013-10-16     Completed Date:  2013-12-06     Revised Date:  2014-10-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1230-7     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Adult
Antioxidants / pharmacology
Ascorbic Acid / pharmacology
Case-Control Studies
Endothelium, Vascular / drug effects,  physiopathology*
Epoprostenol / pharmacology
Humans
Infusions, Intra-Arterial
Metabolic Syndrome X / physiopathology*
Microvessels / drug effects,  physiopathology*
Muscle, Skeletal / blood supply,  ultrasonography
Muscle, Smooth, Vascular / drug effects,  physiopathology*
Nitroprusside / pharmacology
Obesity / physiopathology*
Oxidative Stress*
Regional Blood Flow
Ultrasonography, Doppler
Vasodilation / drug effects,  physiology*
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
HL-091397/HL/NHLBI NIH HHS; HL-105820/HL/NHLBI NIH HHS; R01 HL105820/HL/NHLBI NIH HHS; RR-000167/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Vasodilator Agents; 169D1260KM/Nitroprusside; DCR9Z582X0/Epoprostenol; N9YNS0M02X/Acetylcholine; PQ6CK8PD0R/Ascorbic Acid
Comments/Corrections

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


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