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Early Cellular and Molecular Changes During Hemodynamic Initiation of Intracranial Aneurysms in a Rabbit Model

[+] Author Affiliations
Ling Gao, Max Mandelbaum, Nicholas Liaw, Sabareesh K. Natarajan, Adnan H. Siddiqui, Hui Meng, John Kolega

State University of New York at Buffalo, Buffalo, NY

J. Mocco

State University of New York at Buffalo, Buffalo, NYUniversity of Florida, Gainesville, FL

Paper No. SBC2010-19598, pp. 577-578; 2 pages
doi:10.1115/SBC2010-19598
From:
  • ASME 2010 Summer Bioengineering Conference
  • ASME 2010 Summer Bioengineering Conference, Parts A and B
  • Naples, Florida, USA, June 16–19, 2010
  • Conference Sponsors: Bioengineering Division
  • ISBN: 978-0-7918-4403-8
  • Copyright © 2010 by ASME

abstract

Hemodynamics constitutes a critical factor in the formation of intracranial aneurysms. However, little is known about how an intracranial arterial wall responds to a hemodynamic insult, and how that response contributes to aneurysm formation. Unlike straight arterial segments (which respond to increased flow by expansive remodeling) and sinuses opposing bifurcation apices (which harbor recirculation flows and are prone to atherosclerotic development), aneurysmal degeneration occurs on the apical side of the bifurcation in the immediate peri-apical region, where flow creates very high wall shear stress (WSS) and wall shear stress gradient (WSSG)1. This results in destructive aneurysmal remodeling, characterized by loss of the internal elastic lamina (IEL) and thinning of the media. It is unknown how the unique hemodynamic conditions of combined high WSS and positive WSSG elicit these morphological changes, how the vascular wall responds to such insult at the molecular level, and what molecular mechanisms are involved.

Copyright © 2010 by ASME

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