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The effect of arterial wall shear stress on the incremental elasticity of a conduit artery
Author(s) -
Kelly R. F.,
Snow H. M.
Publication year - 2011
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2010.02245.x
Subject(s) - shear stress , cardiac cycle , artery , cardiology , elasticity (physics) , blood pressure , blood flow , cardiac output , shunt (medical) , medicine , hemodynamics , anatomy , materials science , composite material
Aims: The purpose of this investigation was to determine the effects of flow mediated dilatation on arterial incremental elasticity ( E inc ). Methods: In four female anaesthetized pigs, the iliac artery and vein were connected by a shunt with a variable resistance which allowed blood flow and therefore shear stress to be regulated. E inc was calculated from simultaneous records of diameter and pressure throughout a minimum of four cardiac cycles. Results: Passive increases in diameter (∼1–2%) throughout a cardiac cycle, brought about by pressure, resulted in a two‐ to threefold increase in E inc . In contrast, increases in shear stress caused active smooth muscle relaxation and a significant increase in diameter from 3.663 ± 0.215 mm to 4.488 ± 0.163 mm (mean ± SEM, P < 0.05) equivalent to a fractional increase in diameter (fD) of 1.5 with no significant change in mean arterial pressure, 108 ± 2 mmHg to 106 ± 1 mmHg (mean ± SEM). The average value of E inc per cardiac cycle at baseline was 2.17 ± 0.10 × 10 3 kPa and remained relatively constant until fD exceeded 1.3 thereafter increasing to a maximum of 9.23 ± 1.0 × 10 3 kPa. Conclusion: These results show that in a conduit artery during the dilatory response to shear stress, the interaction between smooth muscle and collagen operates so as to maintain E inc relatively constant over much of the working range of dilatation. This is consistent with a model of the arterial wall in which collagen is recruited both by passive stretch, in response to an increase in pressure and therefore wall stress, and also by active contraction of smooth muscle.