Alberto Coccarelli, Ioannis Polydoros, Alex Drysdale, Osama F Harraz, Chennakesava Kadapa
{"title":"量化肌源性脑动脉网络血流动态的新计算模型。","authors":"Alberto Coccarelli, Ioannis Polydoros, Alex Drysdale, Osama F Harraz, Chennakesava Kadapa","doi":"","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 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.</p>","PeriodicalId":93888,"journal":{"name":"ArXiv","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11601795/pdf/","citationCount":"0","resultStr":"{\"title\":\"A new computational model for quantifying blood flow dynamics across myogenically-active cerebral arterial networks.\",\"authors\":\"Alberto Coccarelli, Ioannis Polydoros, Alex Drysdale, Osama F Harraz, Chennakesava Kadapa\",\"doi\":\"\",\"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 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.</p>\",\"PeriodicalId\":93888,\"journal\":{\"name\":\"ArXiv\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-11-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11601795/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ArXiv\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ArXiv","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
A new computational model 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 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.