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Article: A theoretical model of cerebral hemodynamics: application to the study of arteriovenous malformations

TitleA theoretical model of cerebral hemodynamics: application to the study of arteriovenous malformations
Authors
KeywordsArteriovenous malformation,
Autoregulation
Cerebral hemodynamics
Compartmental flow model
Regional cerebral blood flow
Issue Date1997
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/jcbfm
Citation
Journal of Cerebral Blood Flow and Metabolism, 1997, v. 17 n. 8, p. 905-918 How to Cite?
AbstractA comprehensive computer model of the cerebral circulation, based on both hydrodynamics and electrical network analysis, was used to investigate the influences of arteriovenous malformations (AVM) on regional cerebral hemodynamics. The basic model contained 114 normal compartments: 55 arteries, 37 veins, 20 microvessel groups (MVG), one compartment representing systemic and extracranial vascular resistance, and one representing the heart. Each microvessel group, which represented the arteriolar bed, consisted of 5000 microvessels. Cerebral blood flow autoregulation was simulated by a formula that determined the resistance and therefore the flow rate of the microvessel groups (arterioles) as a function of perfusion pressure. Elasticity was introduced to describe the compliance of each vessel. Flow rate was made a controlling factor for the positive regulation of the diameters of conductance vessels by calculation of shear stress on the vessel wall (vessel dilation). Models containing an AVM were constructed by adding an AVM compartment and its feeding arteries and draining veins. In addition to the basic model, AVM models were simulated with and without autoregulation and flow-induced conductance vessel dilation to evaluate the contributions of these factors on cerebral hemodynamics. Results for the model with vessel dilation were more similar to clinical observations than those without vessel dilation. Even in the presence of total vasoparalysis of the arteriolar bed equivalent, obliteration of a large (1000 mL/min) shunt flow AVM resulted in a near-field CBF increase from a baseline of 21 to a post-occlusion value of no more than 74 mL/100 g/min, casting doubt on a purely hemodynamic basis for severe hyperemia after treatment. The results of the simulations suggest that our model may be a useful tool to study hemodynamic problems of the cerebral circulation.
Persistent Identifierhttp://hdl.handle.net/10722/49031
ISSN
2015 Impact Factor: 4.929
2015 SCImago Journal Rankings: 3.004
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGao, Een_HK
dc.contributor.authorMa, Qen_HK
dc.contributor.authorYoung, WLen_HK
dc.contributor.authorOrnstein, Een_HK
dc.contributor.authorPile-Spellman, Jen_HK
dc.date.accessioned2008-06-12T06:32:45Z-
dc.date.available2008-06-12T06:32:45Z-
dc.date.issued1997en_HK
dc.identifier.citationJournal of Cerebral Blood Flow and Metabolism, 1997, v. 17 n. 8, p. 905-918en_HK
dc.identifier.issn0271-678Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/49031-
dc.description.abstractA comprehensive computer model of the cerebral circulation, based on both hydrodynamics and electrical network analysis, was used to investigate the influences of arteriovenous malformations (AVM) on regional cerebral hemodynamics. The basic model contained 114 normal compartments: 55 arteries, 37 veins, 20 microvessel groups (MVG), one compartment representing systemic and extracranial vascular resistance, and one representing the heart. Each microvessel group, which represented the arteriolar bed, consisted of 5000 microvessels. Cerebral blood flow autoregulation was simulated by a formula that determined the resistance and therefore the flow rate of the microvessel groups (arterioles) as a function of perfusion pressure. Elasticity was introduced to describe the compliance of each vessel. Flow rate was made a controlling factor for the positive regulation of the diameters of conductance vessels by calculation of shear stress on the vessel wall (vessel dilation). Models containing an AVM were constructed by adding an AVM compartment and its feeding arteries and draining veins. In addition to the basic model, AVM models were simulated with and without autoregulation and flow-induced conductance vessel dilation to evaluate the contributions of these factors on cerebral hemodynamics. Results for the model with vessel dilation were more similar to clinical observations than those without vessel dilation. Even in the presence of total vasoparalysis of the arteriolar bed equivalent, obliteration of a large (1000 mL/min) shunt flow AVM resulted in a near-field CBF increase from a baseline of 21 to a post-occlusion value of no more than 74 mL/100 g/min, casting doubt on a purely hemodynamic basis for severe hyperemia after treatment. The results of the simulations suggest that our model may be a useful tool to study hemodynamic problems of the cerebral circulation.en_HK
dc.format.extent418 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/jcbfmen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectArteriovenous malformation,en_HK
dc.subjectAutoregulationen_HK
dc.subjectCerebral hemodynamicsen_HK
dc.subjectCompartmental flow modelen_HK
dc.subjectRegional cerebral blood flowen_HK
dc.titleA theoretical model of cerebral hemodynamics: application to the study of arteriovenous malformationsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0271-678X&volume=17&issue=8&spage=905&epage=918&date=1997&atitle=A+theoretical+model+of+cerebral+hemodynamics:+application+to+the+study+of+arteriovenous+malformationsen_HK
dc.identifier.emailMa, Q: qyma@eee.hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1097/00004647-199708000-00009en_HK
dc.identifier.pmid9290588en_HK
dc.identifier.hkuros26800-
dc.identifier.isiWOS:A1997XU90200009-

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