Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
Arteriosclerosis, Thrombosis, and Vascular Biology. 1989;9:511-522

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Friedman, M. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Friedman, M. H.

Arteriosclerosis, Vol 9, 511-522, Copyright © 1989 by American Heart Association


ARTICLES

A biologically plausible model of thickening of arterial intima under shear

MH Friedman
Biomedical Engineering Center, Ohio State University, Columbus 43210.

A biologically plausible model of the early thickening of the arterial intima has been developed to interpret experimental data relating hemodynamic shear to human intimal morphology. The model included many processes known or commonly believed to take place in the vascular intima, including: smooth muscle cell migration, proliferation, metabolism, and expression of extracellular matrix; lipoprotein kinetics and binding; and monocyte chemotaxis, conversion to macrophage, and foam cell formation. Certain of these processes were allowed to be shear-dependent. The best fit to the data was obtained when smooth muscle cell accumulation was more rapid, and extracellular matrix expression proceeded more slowly where the fluid shear was relatively high and unidirectional. This result is consistent with the earlier inference that competing shear-dependent processes take place in the wall; it is also consistent with the notion that intimal thickening might be part of an adaptive mechanism by which the artery maintains a favorable shear environment.


This article has been cited by other articles:


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
H. C. McGill Jr, C. A. McMahan, E. E. Herderick, R. E. Tracy, G. T. Malcom, A. W. Zieske, and J. P. Strong
Effects of Coronary Heart Disease Risk Factors on Atherosclerosis of Selected Regions of the Aorta and Right Coronary Artery
Arterioscler Thromb Vasc Biol, March 1, 2000; 20(3): 836 - 845.
[Abstract] [Full Text] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
J. Ravensbergen, J. W. Ravensbergen, J. K. B. Krijger, B. Hillen, and H. W. Hoogstraten
Localizing Role of Hemodynamics in Atherosclerosis in Several Human Vertebrobasilar Junction Geometries
Arterioscler Thromb Vasc Biol, May 1, 1998; 18(5): 708 - 716.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
A. Koller and A. Huang
Shear Stress–Induced Dilation Is Attenuated in Skeletal Muscle Arterioles of Hypertensive Rats
Hypertension, April 1, 1995; 25(4): 758 - 763.
[Abstract] [Full Text]