Affiliations: Laboratory of Biomechanics, Center for Experimental Surgery, Foundation of Biomedical Research, Academy of Athens, Athens, Greece | Laboratory of Biofluid Mechanics and Biomedical Engineering, School of Mechanical Engineering, National Technical University, Athens, Greece | Vascular Unit, 3rd Department of Surgery, University Hospital ‘Atticon’, Athens University Medical School, Athens, Greece | Laboratory of Hemodynamics and Cardiovascular Technology, Swiss Federal Institute of Technology (EPFL), Lausanne, Switzerland
Note: [] Address for correspondence: Dr. Dimitrios P. Sokolis, Lefkados St. 35, Athens 15354, Greece. Tel.: +30 210 659 7370; Fax: +30 210 659 7365; E-mail: DimitrisSokolis@ath.forthnet.gr.
Abstract: Numerous studies have provided evidence of diameter adaptation secondary to flow-overload, but with ambiguous findings vis à vis other morphological parameters and information on the biomechanical aspects of arterial adaptation is rather incomplete. We examined the time course of large-artery biomechanical adaptation elicited by long-term flow-overload in a porcine shunt model between the carotid artery and ipsilateral jugular vein. Post-shunting, the proximal artery flow was doubled and retained so until euthanasia (up to three months post-operatively), without pressure change. This hemodynamic stimulus induced lumen diameter enlargement, accommodated by elastin fragmentation and connective tissue accumulation, as witnessed by optical and confocal microscopy. Heterogeneous mass growth of the adventitia was observed at the expense of the media, associated with declining residual strains and opening angle at three months. The in vitro elastic properties of shunted arteries determined by inflation/extension testing were also modified, with the thickness–pressure curves shifted to larger thicknesses and the diameter–pressure curves shifted to larger diameters at physiologic pressures, resulting in normalization of intramural and shear stresses within fifteen and thirty days, respectively. We infer that the biomechanical adaptation in moderate flow-overload leads to normalization of intimal shear, without, however, restoring compliance and distensibility at mean in vivo pressure to control levels.
