title: Modelling of sodium-overload arrhythmias and their suppression.
abstract: Models of the electrophysiological properties of cardiac cells are now capable of accounting not only for normal activity, but also for some of the mechanisms of arrhythmia. A good example is the reconstruction of the inotropic and arrhythmogenic effects of sodium pump inhibition leading to the generation of ectopic beats. The models can also be used to investigate the possible mechanisms of suppression of arrhythmias. The authors show how the antiarrhythmic actions of lidocaine may be reproduced. The results account for the large difference between therapeutic levels (approximately 30 microM) in whole tissue and the concentration (approximately 500 microM) required to suppress excitation in isolated cells.
authors.affiliation: University Laboratory of Physiology, University of Oxford, United Kingdom. denis.noble@physiol.ox.ac.uk
authors.forename: D
authors.initials: D
authors.lastname: Noble
authors.forename: A
authors.initials: A
authors.lastname: Varghese
mesh_terms: D000818:Animals; D005117:Cardiac Complexes, Premature / Q000209:etiology* / Q000503:physiopathology*; D006801:Humans; D006955:Hypernatremia / Q000150:complications* / Q000503:physiopathology*; D008433:Mathematics; D008955:Models, Cardiovascular; D015221:Potassium Channels; D015222:Sodium Channels
chemical_list: D015221:Potassium Channels; D015222:Sodium Channels