A mathematical model for persistent post-CSD vasoconstriction
Cortical spreading depression (CSD) is the propagation of a relatively slow wave in cortical brain tissue that is linked to a number of pathological conditions such as stroke and migraine. Most of the existing literature investigates the dynamics of short term phenomena such as the depolarization an...
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| Veröffentlicht in: | PLoS computational biology 2020-07, Vol.16 (7), p.e1007996-e1007996 |
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| creator | Xu, Shixin Chang, Joshua C Chow, Carson C Brennan, K C Huang, Huaxiong |
| description | Cortical spreading depression (CSD) is the propagation of a relatively slow wave in cortical brain tissue that is linked to a number of pathological conditions such as stroke and migraine. Most of the existing literature investigates the dynamics of short term phenomena such as the depolarization and repolarization of membrane potentials or large ion shifts. Here, we focus on the clinically-relevant hour-long state of neurovascular malfunction in the wake of CSDs. This dysfunctional state involves widespread vasoconstriction and a general disruption of neurovascular coupling. We demonstrate, using a mathematical model, that dissolution of calcium that has aggregated within the mitochondria of vascular smooth muscle cells can drive an hour-long disruption. We model the rate of calcium clearance as well as the dynamical implications on overall blood flow. Based on reaction stoichiometry, we quantify a possible impact of calcium phosphate dissolution on the maintenance of F0F1-ATP synthase activity. |
| doi_str_mv | 10.1371/journal.pcbi.1007996 |
| format | Article |
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Most of the existing literature investigates the dynamics of short term phenomena such as the depolarization and repolarization of membrane potentials or large ion shifts. Here, we focus on the clinically-relevant hour-long state of neurovascular malfunction in the wake of CSDs. This dysfunctional state involves widespread vasoconstriction and a general disruption of neurovascular coupling. We demonstrate, using a mathematical model, that dissolution of calcium that has aggregated within the mitochondria of vascular smooth muscle cells can drive an hour-long disruption. We model the rate of calcium clearance as well as the dynamical implications on overall blood flow. Based on reaction stoichiometry, we quantify a possible impact of calcium phosphate dissolution on the maintenance of F0F1-ATP synthase activity.</description><identifier>ISSN: 1553-7358</identifier><identifier>ISSN: 1553-734X</identifier><identifier>EISSN: 1553-7358</identifier><identifier>DOI: 10.1371/journal.pcbi.1007996</identifier><identifier>PMID: 32667909</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenosine Triphosphate - chemistry ; ATP synthase ; Biology and Life Sciences ; Blood flow ; Brain research ; Calcium ; Calcium - chemistry ; Calcium phosphates ; Calcium Phosphates - chemistry ; Cerebral cortex ; Cerebral Cortex - physiopathology ; Cerebrovascular Circulation ; Cortical Spreading Depression ; Cytosol - chemistry ; Depolarization ; Development and progression ; Disruption ; Dissolution ; Endoplasmic Reticulum - chemistry ; Gray Matter - physiopathology ; Headache ; Health aspects ; Humans ; Laboratories ; Mathematical analysis ; Mathematical models ; Mathematics ; Medicine and Health Sciences ; Membrane potential ; Membrane Potentials ; Metabolism ; Migraine ; Mitochondria ; Mitochondria - metabolism ; Models, Theoretical ; Muscles ; Neurologic manifestations ; Neurovascular Coupling ; Oscillometry ; Oxygen - chemistry ; Permeability ; Phosphorylation ; Physical Sciences ; Physiological aspects ; Physiology ; Proton-Translocating ATPases - chemistry ; Quantitative analysis ; Smooth muscle ; Stoichiometry ; Stroke - physiopathology ; Traumatic brain injury ; Vasoconstriction ; Wave propagation</subject><ispartof>PLoS computational biology, 2020-07, Vol.16 (7), p.e1007996-e1007996</ispartof><rights>COPYRIGHT 2020 Public Library of Science</rights><rights>This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. 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Most of the existing literature investigates the dynamics of short term phenomena such as the depolarization and repolarization of membrane potentials or large ion shifts. Here, we focus on the clinically-relevant hour-long state of neurovascular malfunction in the wake of CSDs. This dysfunctional state involves widespread vasoconstriction and a general disruption of neurovascular coupling. We demonstrate, using a mathematical model, that dissolution of calcium that has aggregated within the mitochondria of vascular smooth muscle cells can drive an hour-long disruption. We model the rate of calcium clearance as well as the dynamical implications on overall blood flow. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS computational biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Shixin</au><au>Chang, Joshua C</au><au>Chow, Carson C</au><au>Brennan, K C</au><au>Huang, Huaxiong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A mathematical model for persistent post-CSD vasoconstriction</atitle><jtitle>PLoS computational biology</jtitle><addtitle>PLoS Comput Biol</addtitle><date>2020-07-01</date><risdate>2020</risdate><volume>16</volume><issue>7</issue><spage>e1007996</spage><epage>e1007996</epage><pages>e1007996-e1007996</pages><issn>1553-7358</issn><issn>1553-734X</issn><eissn>1553-7358</eissn><abstract>Cortical spreading depression (CSD) is the propagation of a relatively slow wave in cortical brain tissue that is linked to a number of pathological conditions such as stroke and migraine. Most of the existing literature investigates the dynamics of short term phenomena such as the depolarization and repolarization of membrane potentials or large ion shifts. Here, we focus on the clinically-relevant hour-long state of neurovascular malfunction in the wake of CSDs. This dysfunctional state involves widespread vasoconstriction and a general disruption of neurovascular coupling. We demonstrate, using a mathematical model, that dissolution of calcium that has aggregated within the mitochondria of vascular smooth muscle cells can drive an hour-long disruption. We model the rate of calcium clearance as well as the dynamical implications on overall blood flow. Based on reaction stoichiometry, we quantify a possible impact of calcium phosphate dissolution on the maintenance of F0F1-ATP synthase activity.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>32667909</pmid><doi>10.1371/journal.pcbi.1007996</doi><orcidid>https://orcid.org/0000-0003-1463-9553</orcidid><orcidid>https://orcid.org/0000-0002-1594-4077</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine Triphosphate - chemistry ATP synthase Biology and Life Sciences Blood flow Brain research Calcium Calcium - chemistry Calcium phosphates Calcium Phosphates - chemistry Cerebral cortex Cerebral Cortex - physiopathology Cerebrovascular Circulation Cortical Spreading Depression Cytosol - chemistry Depolarization Development and progression Disruption Dissolution Endoplasmic Reticulum - chemistry Gray Matter - physiopathology Headache Health aspects Humans Laboratories Mathematical analysis Mathematical models Mathematics Medicine and Health Sciences Membrane potential Membrane Potentials Metabolism Migraine Mitochondria Mitochondria - metabolism Models, Theoretical Muscles Neurologic manifestations Neurovascular Coupling Oscillometry Oxygen - chemistry Permeability Phosphorylation Physical Sciences Physiological aspects Physiology Proton-Translocating ATPases - chemistry Quantitative analysis Smooth muscle Stoichiometry Stroke - physiopathology Traumatic brain injury Vasoconstriction Wave propagation |
| title | A mathematical model for persistent post-CSD vasoconstriction |
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