Alberto Coccarelli, Ioannis Polydoros, Alex Drysdale, Osama F Harraz, Chennakesava Kadapa
{"title":"一个计算框架,用于量化血流动力学跨越肌生成活跃的脑动脉网络。","authors":"Alberto Coccarelli, Ioannis Polydoros, Alex Drysdale, Osama F Harraz, Chennakesava Kadapa","doi":"10.1007/s10237-025-01958-3","DOIUrl":null,"url":null,"abstract":"<p><p>Cerebral autoregulation plays a key physiological role by limiting blood flow changes in the face of pressure fluctuations. Although the underlying vascular cellular processes are chemo-mechanically driven, estimating the associated haemodynamic forces in vivo remains extremely difficult and uncertain. In this work, we propose a novel computational methodology 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 integrates a continuum mechanics-based, biologically-motivated model of the rat vascular wall with 1D blood flow dynamics. We investigate the time dependency of the vascular wall response to pressure changes at both single vessel and network levels. The dynamical performance of the vessel wall mechanics model was validated against different pressure protocols and conditions (control and absence of extracellular <math><msup><mtext>Ca</mtext> <mrow><mn>2</mn> <mo>+</mo></mrow> </msup> </math> ). The robustness of the integrated fluid-structure interaction framework was assessed using different types of inlet signals and numerical settings in an idealized vascular network formed by a middle cerebral artery and its three generations. The proposed in-silico methodology aims to quantify how acute changes in upstream luminal pressure propagate and influence blood flow across a network of rat cerebral arteries. Weak coupling ensured accurate results with a lower computational cost for the vessel size and boundary conditions considered. To complete the analysis, we evaluated the effect of an upstream pressure surge on vascular network haemodynamics in the presence and absence of myogenic tone. This provided a clear quantitative picture of how pressure, flow and vascular constriction are re-distributed across each vessel generation upon inlet pressure changes. This work paves the way for future combined experimental-computational studies aiming to decipher cerebral autoregulation.</p>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":" ","pages":""},"PeriodicalIF":3.0000,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A computational framework for quantifying blood flow dynamics across myogenically-active cerebral arterial networks.\",\"authors\":\"Alberto Coccarelli, Ioannis Polydoros, Alex Drysdale, Osama F Harraz, Chennakesava Kadapa\",\"doi\":\"10.1007/s10237-025-01958-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Cerebral autoregulation plays a key physiological role by limiting blood flow changes in the face of pressure fluctuations. Although the underlying vascular cellular processes are chemo-mechanically driven, estimating the associated haemodynamic forces in vivo remains extremely difficult and uncertain. In this work, we propose a novel computational methodology 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 integrates a continuum mechanics-based, biologically-motivated model of the rat vascular wall with 1D blood flow dynamics. We investigate the time dependency of the vascular wall response to pressure changes at both single vessel and network levels. The dynamical performance of the vessel wall mechanics model was validated against different pressure protocols and conditions (control and absence of extracellular <math><msup><mtext>Ca</mtext> <mrow><mn>2</mn> <mo>+</mo></mrow> </msup> </math> ). The robustness of the integrated fluid-structure interaction framework was assessed using different types of inlet signals and numerical settings in an idealized vascular network formed by a middle cerebral artery and its three generations. The proposed in-silico methodology aims to quantify how acute changes in upstream luminal pressure propagate and influence blood flow across a network of rat cerebral arteries. Weak coupling ensured accurate results with a lower computational cost for the vessel size and boundary conditions considered. To complete the analysis, we evaluated the effect of an upstream pressure surge on vascular network haemodynamics in the presence and absence of myogenic tone. This provided a clear quantitative picture of how pressure, flow and vascular constriction are re-distributed across each vessel generation upon inlet pressure changes. 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A computational framework for quantifying blood flow dynamics across myogenically-active cerebral arterial networks.
Cerebral autoregulation plays a key physiological role by limiting blood flow changes in the face of pressure fluctuations. Although the underlying vascular cellular processes are chemo-mechanically driven, estimating the associated haemodynamic forces in vivo remains extremely difficult and uncertain. In this work, we propose a novel computational methodology 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 integrates a continuum mechanics-based, biologically-motivated model of the rat vascular wall with 1D blood flow dynamics. We investigate the time dependency of the vascular wall response to pressure changes at both single vessel and network levels. The dynamical performance of the vessel wall mechanics model was validated against different pressure protocols and conditions (control and absence of extracellular ). The robustness of the integrated fluid-structure interaction framework was assessed using different types of inlet signals and numerical settings in an idealized vascular network formed by a middle cerebral artery and its three generations. The proposed in-silico methodology aims to quantify how acute changes in upstream luminal pressure propagate and influence blood flow across a network of rat cerebral arteries. Weak coupling ensured accurate results with a lower computational cost for the vessel size and boundary conditions considered. To complete the analysis, we evaluated the effect of an upstream pressure surge on vascular network haemodynamics in the presence and absence of myogenic tone. This provided a clear quantitative picture of how pressure, flow and vascular constriction are re-distributed across each vessel generation upon inlet pressure changes. This work paves the way for future combined experimental-computational studies aiming to decipher cerebral autoregulation.
期刊介绍:
Mechanics regulates biological processes at the molecular, cellular, tissue, organ, and organism levels. A goal of this journal is to promote basic and applied research that integrates the expanding knowledge-bases in the allied fields of biomechanics and mechanobiology. Approaches may be experimental, theoretical, or computational; they may address phenomena at the nano, micro, or macrolevels. Of particular interest are investigations that
(1) quantify the mechanical environment in which cells and matrix function in health, disease, or injury,
(2) identify and quantify mechanosensitive responses and their mechanisms,
(3) detail inter-relations between mechanics and biological processes such as growth, remodeling, adaptation, and repair, and
(4) report discoveries that advance therapeutic and diagnostic procedures.
Especially encouraged are analytical and computational models based on solid mechanics, fluid mechanics, or thermomechanics, and their interactions; also encouraged are reports of new experimental methods that expand measurement capabilities and new mathematical methods that facilitate analysis.