Acidosis in models of cardiac ventricular myocytes
transients during acidosis. These interactions are incorporated into a dynamical model of pH regulation in the myocyte to simulate respiratory acidosis in the heart.
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Veröffentlicht in: | Philosophical transactions of the Royal Society of London. Series A: Mathematical, physical, and engineering sciences physical, and engineering sciences, 2006-05, Vol.364 (1842), p.1171-1186 |
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container_title | Philosophical transactions of the Royal Society of London. Series A: Mathematical, physical, and engineering sciences |
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creator | Crampin, Edmund J Smith, Nicolas P Langham, A. Elise Clayton, Richard H Orchard, Clive H |
description | transients during acidosis. These interactions are incorporated into a dynamical model of pH regulation in the myocyte to
simulate respiratory acidosis in the heart. |
doi_str_mv | 10.1098/rsta.2006.1763 |
format | Article |
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simulate respiratory acidosis in the heart.</description><description>In this paper, we review the experimental findings concerning the effects of acidosis on the action potential and calcium
handling in the cardiac ventricular myocyte, and we present a modelling study that establishes the contribution of the different
effects to altered Ca</description><description>The effects of acidosis on cardiac electrophysiology and excitation–contraction coupling have been studied extensively. Acidosis
decreases the strength of contraction and leads to altered calcium transients as a net result of complex interactions between
protons and a variety of intracellular processes. The relative contributions of each of the changes under acidosis are difficult
to establish experimentally, however, and significant uncertainties remain about the key mechanisms of impaired cardiac function.</description><identifier>ISSN: 1364-503X</identifier><identifier>EISSN: 1471-2962</identifier><identifier>DOI: 10.1098/rsta.2006.1763</identifier><identifier>PMID: 16608702</identifier><language>eng</language><publisher>London: The Royal Society</publisher><subject>Acidosis ; Acidosis - physiopathology ; Action Potentials ; Animals ; Calcium Signaling ; Cardiac Ventricular Myocyte ; Cell membranes ; Cells, Cultured ; Computer Simulation ; Heart Ventricles - chemistry ; Heart Ventricles - cytology ; Heart Ventricles - physiopathology ; Humans ; Hydrogen-Ion Concentration ; Intracellular Calcium Handling ; Mathematical Model ; Membrane Potentials ; Modeling ; Models, Cardiovascular ; Muscle Cells ; Myocardium ; Orchards ; Ph Regulation ; Physiological regulation ; Protons ; Respiratory acidosis ; Ventricular Dysfunction, Left - physiopathology</subject><ispartof>Philosophical transactions of the Royal Society of London. Series A: Mathematical, physical, and engineering sciences, 2006-05, Vol.364 (1842), p.1171-1186</ispartof><rights>Copyright 2006 The Royal Society</rights><rights>2006 The Royal Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c536t-bbf0e44633235a0bef78061e0ddba23a8a4097e1c2e596c2c7b80e7ff239e9773</citedby><cites>FETCH-LOGICAL-c536t-bbf0e44633235a0bef78061e0ddba23a8a4097e1c2e596c2c7b80e7ff239e9773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/25190258$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25190258$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,780,784,832,27924,27925,58021,58254</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16608702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Crampin, Edmund J</creatorcontrib><creatorcontrib>Smith, Nicolas P</creatorcontrib><creatorcontrib>Langham, A. Elise</creatorcontrib><creatorcontrib>Clayton, Richard H</creatorcontrib><creatorcontrib>Orchard, Clive H</creatorcontrib><title>Acidosis in models of cardiac ventricular myocytes</title><title>Philosophical transactions of the Royal Society of London. Series A: Mathematical, physical, and engineering sciences</title><addtitle>PHIL TRANS R SOC A</addtitle><description>transients during acidosis. These interactions are incorporated into a dynamical model of pH regulation in the myocyte to
simulate respiratory acidosis in the heart.</description><description>In this paper, we review the experimental findings concerning the effects of acidosis on the action potential and calcium
handling in the cardiac ventricular myocyte, and we present a modelling study that establishes the contribution of the different
effects to altered Ca</description><description>The effects of acidosis on cardiac electrophysiology and excitation–contraction coupling have been studied extensively. Acidosis
decreases the strength of contraction and leads to altered calcium transients as a net result of complex interactions between
protons and a variety of intracellular processes. The relative contributions of each of the changes under acidosis are difficult
to establish experimentally, however, and significant uncertainties remain about the key mechanisms of impaired cardiac function.</description><subject>Acidosis</subject><subject>Acidosis - physiopathology</subject><subject>Action Potentials</subject><subject>Animals</subject><subject>Calcium Signaling</subject><subject>Cardiac Ventricular Myocyte</subject><subject>Cell membranes</subject><subject>Cells, Cultured</subject><subject>Computer Simulation</subject><subject>Heart Ventricles - chemistry</subject><subject>Heart Ventricles - cytology</subject><subject>Heart Ventricles - physiopathology</subject><subject>Humans</subject><subject>Hydrogen-Ion Concentration</subject><subject>Intracellular Calcium Handling</subject><subject>Mathematical Model</subject><subject>Membrane Potentials</subject><subject>Modeling</subject><subject>Models, Cardiovascular</subject><subject>Muscle Cells</subject><subject>Myocardium</subject><subject>Orchards</subject><subject>Ph Regulation</subject><subject>Physiological regulation</subject><subject>Protons</subject><subject>Respiratory acidosis</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><issn>1364-503X</issn><issn>1471-2962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kT1v1TAUhi1ERT9gZQNl6paLPxLb2ShVW0BFMADqZjnOMfUliS-2A-Tf45CrVh1gsq3znMc-rxF6TvCG4Ea-CjHpDcWYb4jg7BE6IpUgJW04fZz3jFdljdnNITqOcYsxIbymT9Ah4RxLgekRomfGdT66WLixGHwHfSy8LYwOndOm-AljCs5MvQ7FMHszJ4hP0YHVfYRn-_UEfbm8-Hz-trz-ePXu_Oy6NDXjqWxbi6GqOGOU1Rq3YIXEnADuulZTpqWucCOAGAp1ww01opUYhLWUNdAIwU7Q6erdBf9jgpjU4KKBvtcj-CkqLiSnslnAzQqa4GMMYNUuuEGHWRGslpTUkpJaUlJLSrnh5d48tQN09_g-lgywFQh-ziN64yDNauunMObjv7Uv1q5tTD7cWWlNGkxrmevlWncxwe-7ug7f8yxM1OqrrNTNB8nom_ef1FXmX6_8rft2-8sFUA-e8_d248eU_0jln1ZEVlQRIoiyU9-rXWezgvxX4eddljxoZn8AmBW1fA</recordid><startdate>20060515</startdate><enddate>20060515</enddate><creator>Crampin, Edmund J</creator><creator>Smith, Nicolas P</creator><creator>Langham, A. Elise</creator><creator>Clayton, Richard H</creator><creator>Orchard, Clive H</creator><general>The Royal Society</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20060515</creationdate><title>Acidosis in models of cardiac ventricular myocytes</title><author>Crampin, Edmund J ; Smith, Nicolas P ; Langham, A. Elise ; Clayton, Richard H ; Orchard, Clive H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c536t-bbf0e44633235a0bef78061e0ddba23a8a4097e1c2e596c2c7b80e7ff239e9773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acidosis</topic><topic>Acidosis - physiopathology</topic><topic>Action Potentials</topic><topic>Animals</topic><topic>Calcium Signaling</topic><topic>Cardiac Ventricular Myocyte</topic><topic>Cell membranes</topic><topic>Cells, Cultured</topic><topic>Computer Simulation</topic><topic>Heart Ventricles - chemistry</topic><topic>Heart Ventricles - cytology</topic><topic>Heart Ventricles - physiopathology</topic><topic>Humans</topic><topic>Hydrogen-Ion Concentration</topic><topic>Intracellular Calcium Handling</topic><topic>Mathematical Model</topic><topic>Membrane Potentials</topic><topic>Modeling</topic><topic>Models, Cardiovascular</topic><topic>Muscle Cells</topic><topic>Myocardium</topic><topic>Orchards</topic><topic>Ph Regulation</topic><topic>Physiological regulation</topic><topic>Protons</topic><topic>Respiratory acidosis</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Crampin, Edmund J</creatorcontrib><creatorcontrib>Smith, Nicolas P</creatorcontrib><creatorcontrib>Langham, A. 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simulate respiratory acidosis in the heart.</abstract><abstract>In this paper, we review the experimental findings concerning the effects of acidosis on the action potential and calcium
handling in the cardiac ventricular myocyte, and we present a modelling study that establishes the contribution of the different
effects to altered Ca</abstract><abstract>The effects of acidosis on cardiac electrophysiology and excitation–contraction coupling have been studied extensively. Acidosis
decreases the strength of contraction and leads to altered calcium transients as a net result of complex interactions between
protons and a variety of intracellular processes. The relative contributions of each of the changes under acidosis are difficult
to establish experimentally, however, and significant uncertainties remain about the key mechanisms of impaired cardiac function.</abstract><cop>London</cop><pub>The Royal Society</pub><pmid>16608702</pmid><doi>10.1098/rsta.2006.1763</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; JSTOR Mathematics & Statistics; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
subjects | Acidosis Acidosis - physiopathology Action Potentials Animals Calcium Signaling Cardiac Ventricular Myocyte Cell membranes Cells, Cultured Computer Simulation Heart Ventricles - chemistry Heart Ventricles - cytology Heart Ventricles - physiopathology Humans Hydrogen-Ion Concentration Intracellular Calcium Handling Mathematical Model Membrane Potentials Modeling Models, Cardiovascular Muscle Cells Myocardium Orchards Ph Regulation Physiological regulation Protons Respiratory acidosis Ventricular Dysfunction, Left - physiopathology |
title | Acidosis in models of cardiac ventricular myocytes |
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