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David A. Eisner
Researcher at University of Manchester
Publications - 267
Citations - 14383
David A. Eisner is an academic researcher from University of Manchester. The author has contributed to research in topics: Ryanodine receptor & Calcium. The author has an hindex of 69, co-authored 256 publications receiving 13473 citations. Previous affiliations of David A. Eisner include University of Oxford & Research Triangle Park.
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Comparison of the effects of caffeine and other methylxanthines on [Ca2+]i in rat ventricular myocytes
TL;DR: It is concluded that many of the differences in the effects of these methylxanthines can be attributed to differences in membrane permeability due to Differences in oil:water partition.
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Increased Vulnerability to Atrial Fibrillation Is Associated With Increased Susceptibility to Alternans in Old Sheep
Charles M. Pearman,George W.P. Madders,Emma J. Radcliffe,Graeme Kirkwood,Michael Lawless,Amy Watkins,Charlotte E.R. Smith,Andrew W. Trafford,David A. Eisner,Katharine M. Dibb +9 more
TL;DR: It is shown, for the first time in a large mammalian model, that aging is associated with increased duration of AF and susceptibility to AP alternans, and it is suggested that instabilities in Ca2+ handling initiate alternan at low stimulation rates, but that AP restitution alone can sustain alternans at higher rates.
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The action of adrenaline on pace-maker activity in cardiac Purkinje fibres
TL;DR: A computer simulation shows that adrenaline can shift the maximum diastolic potential in the hyperpolarizing or depolarizing direction depending on the initial value of [K+]o, which will add to the increase in rate caused by the positive shift of the activation curve for iK2 (the s infinite shift).
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Effects of membrane potential on intracellular calcium concentration in sheep Purkinje fibres in sodium‐free solutions.
TL;DR: The results support the hypothesis that, in Na+‐containing solutions, the increase of tonic tension on depolarization results from a voltage‐dependent Na+•Ca2+ exchange and show, in contrast to previous work, that inNa+‐free solutions toni tension is still sensitive to membrane potential.
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Strophanthidin-induced gain of Ca2+ occurs during diastole and not systole in guinea-pig ventricular myocytes.
TL;DR: The primary mechanism by which the cardiac cell gains Ca2+ when the Na-K pump is inhibited is by a net influx during diastole, which suggests that changes of Ca2- flux during systole are not responsible for the strophanthidin-induced increase of s.r. r. Ca2+.