ArticleArXiv2024
A new computational model for quantifying blood flow dynamics across myogenically-active cerebral arterial networks.
Article in ArXiv, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Updated by
Authors and funding
5 authors.
Funding
Abstract
Cerebral autoregulation plays a key physiological role by limiting blood flow changes in the face of pressure fluctuations. Although the involved cellular processes are mechanically driven, the quantification of haemodynamic forces in in-vivo settings remains extremely difficult and uncertain. In this work, we propose a novel computational framework for evaluating the blood flow dynamics across networks of myogenically active cerebral arteries, which can modulate their muscular tone to stabilize flow (and perfusion pressure) as well as to limit vascular intramural stress. The introduced framework is built on contractile (myogenically active) vascular wall mechanics and blood flow dynamics models, which can be numerically coupled in either a weak or strong way. We investigate the time dependency of the vascular wall response to pressure changes at both single vessel and network levels. The robustness of the model was assessed by considering different types of inlet signals and numerical settings in an idealized vascular network formed by a middle cerebral artery and its three generations. For the vessel size and boundary conditions considered, weak coupling ensured accurate results with a lower computational cost. To complete the analysis, we evaluated the effect of an upstream pressure surge on the haemodynamics of the vascular network. This provided a clear quantitative picture of how pressure and flow are redistributed across each vessel generation upon inlet pressure changes. This work paves the way for future combined experimental-computational studies aiming to decipher cerebral autoregulation.
Identifiers
39606730PMC11601795What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.