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Journal ArticleDOI

Interval-dependent effects of small antiarrhythmic drugs on excitability of guinea-pig myocardium.

Kenneth R. Courtney
- 01 Nov 1980 - 
- Vol. 12, Iss: 11, pp 1273-1286
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TLDR
Myocardial depressant actions of seven antiarrhythmic drugs have been studied in vitro in guinea-pig papillary muscle preparations, using upstroke velocity of action potentials as a measure of myocardial excitability.
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This article is published in Journal of Molecular and Cellular Cardiology.The article was published on 1980-11-01. It has received 133 citations till now. The article focuses on the topics: Procainamide.

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Citations
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Antiarrhythmic Agents: The Modulated Receptor Mechanism of Action of Sodium and Calcium Channel-Blocking Drugs

TL;DR: This review concentrates on the antiarrhythmic drug literature pertinent to an evaluation of the modulated receptor hypothesis: lidocaine, procainamide, quinidine, diphenylhydantoin, and propranolol.
Journal ArticleDOI

Antiarrhythmic drug action. Blockade of the inward sodium current.

TL;DR: The mechanism of the blockade of the sodium current is focused on, which is probably a major mechanism of action of antiarrhythmic drugs.
Journal ArticleDOI

Effects of flecainide and quinidine on human atrial action potentials : role of rate-dependence and comparison with guinea pig, rabbit, and dog tissues

TL;DR: The salutary response of atrial fibrillation to flecainide may be due to enhancement of drug action by the rapid atrial activation rates characteristic of this arrhythmia.
Journal ArticleDOI

Antiarrhythmic agents: modulated receptor applications.

L M Hondeghem
- 01 Mar 1987 - 
TL;DR: The present essay is limited to discussion of sodium-channel blockers and how their time and voltage-dependent block can contribute to antiarrhythmic and arrhythmogenic actions.
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Sodium current depression by lidocaine and quinidine in isolated ventricular cells

TL;DR: These results provide direct evidence that therapeutic doses (10–20 μM) of lidocaine or quinidine strongly inhibit INa, and give some clues about the mechanism of this inhibition.
References
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Book

Substituent constants for correlation analysis in chemistry and biology

TL;DR: In this paper, the book is the window to get in the world and you can open the world easily, and these wise words are really familiar with you, so bring home now the book enPDFd substituent constants for correlation analysis in chemistry and biology to be your sources when going to read.
Journal ArticleDOI

Local anesthetics: hydrophilic and hydrophobic pathways for the drug-receptor reaction.

TL;DR: The results are interpreted in terms of a single receptor in Na channels for the different drug types, and any drug form in the channel increases the probability of closing the inactivation gate which, in effect, is equivalent to a negative shift of the voltage dependence of inactivation.
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Time- and voltage-dependent interactions of antiarrhythmic drugs with cardiac sodium channels.

TL;DR: A molecular model on the action of local anesthetic-like antiarrhytmic drugs is formulated: the drugs can interact with the sodium channels in the rested, activated and inactivated states, and each of these interactions is characterized by an association and dissociation rate constant.
Journal ArticleDOI

The inhibition of sodium currents in myelinated nerve by quaternary derivatives of lidocaine

TL;DR: The inhibition of sodium currents by quaternary derivatives of lidocaine was studied in single myelinated nerve fibers and suggests that the drug binds at a site which is about halfway down the electrical gradient from inside to outside of the sodium channel.
Journal ArticleDOI

Effect of lidocaine and quinidine on steady-state characteristics and recovery kinetics of (dV/dt)max in guinea pig ventricular myocardium.

TL;DR: The study indicates that the mechanisms whereby quinidine and lidocaine influence (dV/dt)max are different and it is possible that this difference may underlie some of the differences in the clinical effects of these two drugs.
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