A simplified fluid–structure model for arterial flow. Application to retinal hemodynamics

Aletti, Matteo; Gerbeau, Jean-Frédéric; Lombardi, Damiano

doi:10.1016/j.cma.2016.03.044

Cited by 8 publications

(4 citation statements)

References 24 publications

(49 reference statements)

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“…Therefore, we used computational modeling to simulate the pressure distribution in different parts of the microvasculature in the retina. We used an established mathematical model of an artery/arteriolar human retinal network in which mural cells are implemented as fibers in the vascular wall 30,31 (Fig. 7A).…”

Section: Hypermuscularization Of the Ts Cripples The Pressure Drop Inmentioning

confidence: 99%

Reducing Hypermuscularization of the Transitional Segment Between Arterioles and Capillaries Protects Against Spontaneous Intracerebral Hemorrhage

et al. 2020

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Background: Spontaneous deep intracerebral hemorrhage (ICH) is a devastating subtype of stroke without specific treatments. It has been thought that smooth muscle cell (SMC) degeneration at the site of arteriolar wall rupture may be sufficient to cause hemorrhage. However, deep ICHs are rare in some aggressive small vessel diseases that are characterized by significant arteriolar SMC degeneration. Here we hypothesized that a second cellular defect may be required for the occurrence of ICH. Methods: We studied a genetic model of spontaneous deep ICH using Col4a1 +/G498V and Col4a1 +/G1064D mouse lines that are mutated for the alpha1 chain of Collagen type IV. We performed high resolution imaging and molecular analyses of cerebroretinal microvessels, genetic rescue experiments, vascular reactivity analysis and computational modeling. We also examined post-mortem brain tissues from patients with sporadic deep ICH. Results: We identified in the normal cerebroretinal vasculature a novel segment between arterioles and capillaries, herein called the transitional segment (TS), that is covered by mural cells distinct from SMCs and pericytes. In Col4a1 mutant mice, this TS was hypermuscularized, with a hyperplasia of mural cells expressing more contractile proteins, whereas the upstream arteriole exhibited a loss of SMCs. Mechanistically, TS showed a transient increase in proliferation of mural cells during post-natal maturation. Mutant brain microvessels, unlike mutant arteries, displayed a significant upregulation of SM genes and Notch3 target genes, and genetic reduction of Notch3 in Col4a1 +/G498V mice protected against ICH. Retina analysis showed that hypermuscularization of the TS was attenuated but arteriolar SMC loss unchanged in Col4a1 +/G498V , Notch3 +/mice. Moreover, hypermuscularization of the retinal TS increased its contractility and tone and raised the intravascular pressure in the upstream feeding arteriole. Consistently, we similarly found

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Section: Hypermuscularization Of the Ts Cripples The Pressure Drop Inmentioning

confidence: 99%

Reducing Hypermuscularization of the Transitional Segment Between Arterioles and Capillaries Protects Against Spontaneous Intracerebral Hemorrhage

et al. 2020

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“…The Navier-Stokes equations were used to find flow within the arterioles, while peripheral circulation was accounted for by an impedance condition at the outlets of the segmented tree. The deformation of vessels caused by the pulse of blood is a computationally complex mechanism to model and a simplified model has been developed and applied to a similar reproduction of the retinal vasculature, with a brief analysis of its effects on haemodynamics [6]. Notably, Rebhan et al have considered the interactions of retinal haemodynamics and tissue stress using reproductions of the large vessels of healthy and diseased eyes, an aspect previously overlooked that may have importance in, e.g.…”

Section: Oxygen Transport and Spatial Modelsmentioning

confidence: 99%

Advancing treatment of retinal disease through in silico trials

2023

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Treating retinal diseases to prevent sight loss is an increasingly important challenge. Thanks to the configuration of the eye, the retina can be examined relatively easily in situ. Owing to recent technological development in scanning devices, much progress has been made in understanding the structure of the retina and characterising retinal biomarkers. However, treatment options remain limited and are often of low efficiency and efficacy.In recent years, the concept of in silico clinical trials has been adopted by many pharmaceutical companies to optimise and accelerate the development of therapeutics. In silico clinical trials rely on the use of mathematical models based on the physical and biochemical mechanisms underpinning a biological system. With appropriate simplifications and assumptions, one can generate computer simulations of various treatment regimens, new therapeutic molecules, delivery strategies and so forth, rapidly and at a fraction of the cost required for the equivalent experiments. Such simulations have the potential not only to hasten the development of therapies and strategies but also tooptimise the use of existing therapeutics.In this paper, we review the state-of-the-art in in silico models of the retina for mathematicians, biomedical scientists and clinicians, highlighting the challenges to developing in silico clinical trials. Throughout this paper, we highlight key findings from in silico models about the physiology of the retina in health and disease. We describe the main building blocks of in silico clinical trials and identify challenges to developing in silico clinical trials of retinal diseases.

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“…This has been proposed and analysed in (Figueroa et al, 2006;Nobile and Vergara, 2008;Colciago et al, 2014;Pironneau, 2014;Chacon-Rebollo et al, 2014). In (Aletti et al, 2016) a modification of the method proposed in (Nobile and Vergara, 2008) is presented, in which we added a set of fibres to mimic the presence of smooth muscle cells. This makes it possible to describe arteriole mechanics and to simulate the phenomenon of autoregulation.…”

Section: Direct Problemsmentioning

confidence: 99%