Document Detail


Time course of carotid artery growth and remodeling in response to altered pulsatility.
MedLine Citation:
PMID:  20852047     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Elucidating early time courses of biomechanical responses by arteries to altered mechanical stimuli is paramount to understanding and eventually predicting long-term adaptations. In a previous study, we reported marked long-term (at 35-56 days) consequences of increased pulsatile hemodynamics on arterial structure and mechanics. Motivated by those findings, we focus herein on arterial responses over shorter periods (at 7, 10, and 14 days) following placement of a constrictive band on the aortic arch between the innominate and left carotid arteries of wild-type mice, which significantly increases pulsatility in the right carotid artery. We quantified hemodynamics in vivo using noninvasive ultrasound and measured wall properties and composition in vitro using biaxial mechanical testing and standard (immuno)histology. Compared with both baseline carotid arteries and left carotids after banding, right carotids after banding experienced a significant increase in both pulse pressure, which peaked at day 7, and a pulsatility index for velocity, which continued to rise over the 42-day study despite a transient increase in mean flow that peaked at day 7. Wall thickness and inner diameter also increased significantly in the right carotids, both peaking at day 14, with an associated marked early reduction in the in vivo axial stretch and a persistent decrease in smooth muscle contractility. Glycosaminoglycan content also increased within the wall, peaking at day 14, whereas increases in monocyte chemoattractant protein-1 activity and the collagen-to-elastin ratio continued to rise. These findings confirm that pulsatility is an important modulator of wall geometry, structure, and properties but reveal different early time courses for different microscopic and macroscopic metrics, presumably due to the separate degrees of influence of pressure and flow.
Authors:
John F Eberth; Natasa Popovic; Vincent C Gresham; Emily Wilson; Jay D Humphrey
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-09-17
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-03     Completed Date:  2011-01-13     Revised Date:  2013-05-27    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1875-83     Citation Subset:  IM    
Affiliation:
Department of Engineering Technology, University of Houston, Houston, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Biomechanics
Blood Pressure*
Carotid Artery, Common / growth & development*,  metabolism,  physiopathology,  ultrasonography
Chemokine CCL2 / metabolism
Collagen / metabolism
Disease Models, Animal
Elasticity
Elastin / metabolism
Glycosaminoglycans / metabolism
Hypertension / metabolism,  physiopathology*,  ultrasonography
Immunohistochemistry
Male
Mechanotransduction, Cellular*
Mice
Mice, 129 Strain
Mice, Inbred C57BL
Muscle, Smooth, Vascular / growth & development,  physiopathology
Pulsatile Flow*
Regional Blood Flow
Time Factors
Grant Support
ID/Acronym/Agency:
HL-64372/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Ccl2 protein, mouse; 0/Chemokine CCL2; 0/Glycosaminoglycans; 9007-34-5/Collagen; 9007-58-3/Elastin
Comments/Corrections

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


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