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
Hauptverfasser: Crampin, Edmund J, Smith, Nicolas P, Langham, A. Elise, Clayton, Richard H, Orchard, Clive H
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container_end_page 1186
container_issue 1842
container_start_page 1171
container_title Philosophical transactions of the Royal Society of London. Series A: Mathematical, physical, and engineering sciences
container_volume 364
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
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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. 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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. 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These interactions are incorporated into a dynamical model of pH regulation in the myocyte to 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. 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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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