Competition between collateral vessels

Keenan, Robert L.; Rodbard, Simon

doi:10.1093/cvr/7.5.670

Cited by 11 publications

(5 citation statements)

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“…While the reduction to a single vessel to reduce energy is a wellestablished phenomenon (Keenan and Rodbard 1973), our novel CFD-coupled optimization based model demonstrates that θ OT is an important factor in selecting the dominant arch due to its role in distributing blood flow. Our power + diffusion simulations suggest that the multi-arch configuration is due to functional objective functions such as metabolic demand.…”

Section: Change In Objective Function Competition Among Parallel Arcmentioning

confidence: 94%

“…Examining a simple network of two parallel vessels, Keenan and Rodbard demonstrated that vascular adaption to τ w alone causes one vessel to enlarge and the other to disappear (Keenan and Rodbard 1973). In their model, vessel caliber increased or reduced to restore "optimal" τ w conditions, effectively minimizing total energy.…”

Section: Change In Objective Function Competition Among Parallel Arcmentioning

confidence: 99%

“…When applying both τ w and metabolic controls, a stable network was achieved, whereas τ w alone again resulted in instability and rarefaction. The target τ w level in this model was not constant as in (Keenan and Rodbard 1973), but varied according to transmural pressure, as suggested by (Pries et al 1995) and incorporated into our model through vessel wall maintenance (Taber 1998b). Applying their model to more complex networks demonstrated that convergence to the in vivo topology could only be obtained by enforcing both τ w and metabolic controls (Pries et al 2001).…”

Section: Change In Objective Function Competition Among Parallel Arcmentioning

confidence: 99%

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Computational hemodynamic optimization predicts dominant aortic arch selection is driven by embryonic outflow tract orientation in the chick embryo

Kowalski

Teslovich

Dur

et al. 2012

Biomech Model Mechanobiol

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In the early embryo, a series of symmetric, paired vessels, the aortic arches, surround the foregut and distribute cardiac output to the growing embryo and fetus. During embryonic development the arch vessels undergo large-scale asymmetric morphogenesis to form species-specific adult great vessel patterns. These transformations occur within a dynamic biomechanical environment, which can play an important role in the development of normal arch configurations or the aberrant arch morphologies associated with congenital cardiac defects. Arrested migration and rotation of the embryonic outflow tract during late stages of cardiac looping has been shown to produce both outflow tract and several arch abnormalities. Here we investigate how changes in flow distribution

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Section: Change In Objective Function Competition Among Parallel Arcmentioning

confidence: 94%

Section: Change In Objective Function Competition Among Parallel Arcmentioning

confidence: 99%

Section: Change In Objective Function Competition Among Parallel Arcmentioning

confidence: 99%

See 1 more Smart Citation

Computational hemodynamic optimization predicts dominant aortic arch selection is driven by embryonic outflow tract orientation in the chick embryo

Kowalski

Teslovich

Dur

et al. 2012

Biomech Model Mechanobiol

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“…The number of veins also declines. We have examined the special case of two vessels that supply equal quantities of blood to a single vascular bed [84] (fig. 18, 19).…”

Section: Reduction Of Calibermentioning

confidence: 99%

Vascular Caliber

Rodbard¹

1975

Cardiology

232

135

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Many aspects of vascular caliber can be accounted for on the basis of interactions between the frictional drag generated by the stream, and the sensitivity of the endothelial cells to this force. When the drag force on endothelial cells is at its critical set-point, these lining cells are at rest with respect to factors that affect caliber. An increase in flow rate increases the drag and appears to induce the endothelium to generate a signal that triggers relaxation of the subjacent medial smooth muscle. The resulting functional dilatation of the vessel reduces the stream velocity and returns the drag to its set-point. If the drag stimulus is persistent or recurrent, vasodilatation is soon followed by anatomical reorganization of the vessel around its enlarged lumen. This sequence can account for gradual, generalized and regional vascular growth, and for the opening of collateral vessels. This sequence may also play a role in the enlargement of veins, lymphatics, airways and other vessels. Turbulence greatly increases drag per unit volume of flow. Aneurysms and and post-stenotic dilatations are considered to result from an increased drag. Jets increase drag to an even greater extent and may account for saccular aneurysms and for ‘jet lesions’. Conversely, reduced flow diminishes drag and thereby triggers constriction of the vascular smooth muscle. Persistent reduction of drag permits proliferation of the subendothelial connective tissue, which reduces vascular caliber until the drag on the lining cells is returned to its set-point. Progressive localized narrowings (stenoses) may also be attributed to a reduced drag. Thus high velocity flow around an irregularity such as a plaque may separate the streamlines from the wall at the downstream end of the narrowing. In this region of separation the cells respond to the reduced local flow and drag by subendothelial proliferation and ingrowth, producing further narrowing. These mechanisms may be operative in

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“…The outflow tract orientation acted to preferentially direct flow to one of the AA vessels, which became the dominant AA. This model showed similarities to the classic problem of competing collateral vessels, where small perturbations in the distribution of blood flow cause one vessel to dilate due to increased WSS while the others constrict due to a decrease in WSS, eventually leading to reduction to a single vessel [63], [64], [65]. Based on this work, the asymmetry observed in AA IV flow at stage 21 (right-lateral dominant, Figure 4) may explain the asymmetric growth of this AA pair, where the left lateral disappears and the right lateral forms a section of the mature arch of aorta.…”

Section: Discussionmentioning

confidence: 81%

Critical Transitions in Early Embryonic Aortic Arch Patterning and Hemodynamics

et al. 2013

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Transformation from the bilaterally symmetric embryonic aortic arches to the mature great vessels is a complex morphogenetic process, requiring both vasculogenic and angiogenic mechanisms. Early aortic arch development occurs simultaneously with rapid changes in pulsatile blood flow, ventricular function, and downstream impedance in both invertebrate and vertebrate species. These dynamic biomechanical environmental landscapes provide critical epigenetic cues for vascular growth and remodeling. In our previous work, we examined hemodynamic loading and aortic arch growth in the chick embryo at Hamburger-Hamilton stages 18 and 24. We provided the first quantitative correlation between wall shear stress (WSS) and aortic arch diameter in the developing embryo, and observed that these two stages contained different aortic arch patterns with no inter-embryo variation. In the present study, we investigate these biomechanical events in the intermediate stage 21 to determine insights into this critical transition. We performed fluorescent dye microinjections to identify aortic arch patterns and measured diameters using both injection recordings and high-resolution optical coherence tomography. Flow and WSS were quantified with 3D computational fluid dynamics (CFD). Dye injections revealed that the transition in aortic arch pattern is not a uniform process and multiple configurations were documented at stage 21. CFD analysis showed that WSS is substantially elevated compared to both the previous (stage 18) and subsequent (stage 24) developmental time-points. These results demonstrate that acute increases in WSS are followed by a period of vascular remodeling to restore normative hemodynamic loading. Fluctuations in blood flow are one possible mechanism that impacts the timing of events such as aortic arch regression and generation, leading to the variable configurations at stage 21. Aortic arch variations noted during normal rapid vascular remodeling at stage 21 identify a temporal window of increased vulnerability to aberrant aortic arch morphogenesis with the potential for profound effects on subsequent cardiovascular morphogenesis.

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Competition between collateral vessels

Cited by 11 publications

References 0 publications

Computational hemodynamic optimization predicts dominant aortic arch selection is driven by embryonic outflow tract orientation in the chick embryo

Computational hemodynamic optimization predicts dominant aortic arch selection is driven by embryonic outflow tract orientation in the chick embryo

Vascular Caliber

Critical Transitions in Early Embryonic Aortic Arch Patterning and Hemodynamics

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