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Review
. 2015 Oct;26(5):376-83.
doi: 10.1097/MOL.0000000000000218.

Blood flow modulation of vascular dynamics

Affiliations
Review

Blood flow modulation of vascular dynamics

Juhyun Lee et al. Curr Opin Lipidol. 2015 Oct.

Abstract

Purpose of review: Blood flow is intimately linked with cardiovascular development, repair and dysfunction. The current review will build on the fluid mechanical principle underlying haemodynamic shear forces, mechanotransduction and metabolic effects.

Recent findings: Pulsatile flow produces both time (∂τ/∂t) and spatial-varying shear stress (∂τ/∂x) to modulate vascular oxidative stress and inflammatory response with pathophysiological significance to atherosclerosis. The characteristics of haemodynamic shear forces, namely, steady laminar (∂τ/∂t = 0), pulsatile shear stress (PSS: unidirectional forward flow) and oscillatory shear stress (bidirectional with a near net 0 forward flow), modulate mechano-signal transduction to influence metabolic effects on vascular endothelial function. Atheroprotective PSS promotes antioxidant, anti-inflammatory and antithrombotic responses, whereas atherogenic oscillatory shear stress induces nicotinamide adenine dinucleotide phosphate oxidase-JNK signalling to increase mitochondrial superoxide production, protein degradation of manganese superoxide dismutase and post-translational protein modifications of LDL particles in the disturbed flow-exposed regions of vasculature. In the era of tissue regeneration, shear stress has been implicated in reactivation of developmental genes, namely, Wnt and Notch signalling, for vascular development and repair.

Summary: Blood flow imparts a dynamic continuum from vascular development to repair. Augmentation of PSS confers atheroprotection and reactivation of developmental signalling pathways for regeneration.

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Conflict of interest statement

Conflicts of interest: We have no conflicts of interest.

Figures

Figure 1
Figure 1
(a) Shear stress profiles at the lateral and medial walls of arterial bifurcations. (b) Pulsatile shear stress (PSS) occurs at the medial wall (red circle), whereas oscillating flow (OSS) occurs at the migrating stagnation point of the lateral wall (blue circle). (c) Flow separation and disturbed flow develops at the lateral wall. (d) Angiogram supports the predilection sites for atherosclerosis. (e) Spatial variations in wall shear stress profiles at an instantaneous moment in systole. The magnitude of wall shear stress is relatively high in the ascending aorta, greater curvature, and descending aorta. Cross-section at the aortic arch reveals an eccentric distribution of high shear stress in the greater curvature but low in the lesser curvature. Cross-section from the descending aorta reveals concentric high shear stress.
Figure 2
Figure 2
Comparison between Couette and Poiseuille flow. (a) When top plate moves with velocity U and bottom plate is fixed, fluid motion (Navier-Stoke Equation) shows a linear profile. Also, shear stress profile shows the constant profile. (b) When constant pressure is applied to fluid which is trapped between two fixed plates, fluid motion shows a parabolic flow. Shear stress profile shows a linear profile. Anatomic variation promotes low reversal occurring from the high pressured to low pressured regions. (c) In the bifurcated region, low pressure develops at the lateral wall of bifurcation, lesser curvature, and the post-stenotic region. (d) In the wake of post-stenotic region, low pressure promotes flow separation and flow reversal. (e) In aortic arch, Greater curvature has higher pressure than the lesser curvature.
Figure 3
Figure 3
Oscillatory shear stress mediated mechanotranduction signal modulates inflammatory responses, whereas pulsatile shear stress activates G-protein and PIP3-AKT pathway, leading to phosphoyrylation of eNOS.

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References

    1. Madamanchi NR, Vendrov A, Runge MS. Oxidative stress and vascular disease. Arteriosclerosis, thrombosis, and vascular biology. 2005;25:29–38. - PubMed
    1. Harrison D, Griendling KK, Landmesser U, et al. Role of oxidative stress in atherosclerosis. The American journal of cardiology. 2003;91:7A–11A. - PubMed
    1. Hwang J, Ing MH, Salazar A, et al. Pulsatile versus oscillatory shear stress regulates NADPH oxidase subunit expression: implication for native LDL oxidation. Circ Res. 2003;93:1225–1232. - PMC - PubMed
    1. Li R, Mittelstein D, Lee J, et al. A dynamic model of calcific nodule destabilization in response to monocyte- and oxidized lipid-induced matrix metalloproteinases. American journal of physiology Cell physiology. 2012;302:C658–665. - PMC - PubMed
    1. Stone PH, Coskun AU, Kinlay S, et al. Effect of endothelial shear stress on the progression of coronary artery disease, vascular remodeling, and in-stent restenosis in humans: in vivo 6-month follow-up study. Circulation. 2003;108:438–444. - PubMed

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