Experimental modeling of sudden death pathological mechanisms in Na+ channel blocker treatment

In laboratory rats, a minimal arrhythmogenic dose of 1, 5 % KCl solution (15 mg/kg) was injected intravenously in 2 seconds. Hypopolarization arrhythmias were registered in 3-10 seconds, followed by regular sinus rhythm. In experimental groups, the animals received a minimal arrhythmogenic dose of K...

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Main Authors: V. M. Moroz, T. N. Lipnitsky
Format: Article
Language:Russian
Published: «FIRMA «SILICEA» LLC  2006-06-01
Series:Российский кардиологический журнал
Subjects:
Online Access:https://russjcardiol.elpub.ru/jour/article/view/1842
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spelling doaj-793233ef27d94f49a0a9a35c91f8de7c2021-07-28T14:02:08Zrus«FIRMA «SILICEA» LLC Российский кардиологический журнал1560-40712618-76202006-06-010367701603Experimental modeling of sudden death pathological mechanisms in Na+ channel blocker treatmentV. M. Moroz0T. N. Lipnitsky1Винницкий национальный медицинский университетВинницкий национальный медицинский университетIn laboratory rats, a minimal arrhythmogenic dose of 1, 5 % KCl solution (15 mg/kg) was injected intravenously in 2 seconds. Hypopolarization arrhythmias were registered in 3-10 seconds, followed by regular sinus rhythm. In experimental groups, the animals received a minimal arrhythmogenic dose of KCl in 5 minutes after intravenous infusion of 1 % novocainamidum (20 mg/kg) or 0, 25 % ethacyzin (4 mg/kg). In all 20 rats, N a+ cannel blocker and KCl bolus administration resulted in cardioplegy; in every second animal, asystolia and death were registered (40 % and 60 %, respectively). Therefore, in coronary heart disease patients, receiving Na+ channel blockers, sudden death pathogenesis might be influenced by membrane hyperpolarization, due to Na+/K+-ATPase dysfunction, low cytosol concentration of K+ ions, and their decreased flow from the cells in final repolarization phase.https://russjcardiol.elpub.ru/jour/article/view/1842sudden deathcardiac arrhythmiasmembrane hyperpolarizationhyperkaliemiaarrhythmogenic effects of antiarrhythmics
collection DOAJ
language Russian
format Article
sources DOAJ
author V. M. Moroz
T. N. Lipnitsky
spellingShingle V. M. Moroz
T. N. Lipnitsky
Experimental modeling of sudden death pathological mechanisms in Na+ channel blocker treatment
Российский кардиологический журнал
sudden death
cardiac arrhythmias
membrane hyperpolarization
hyperkaliemia
arrhythmogenic effects of antiarrhythmics
author_facet V. M. Moroz
T. N. Lipnitsky
author_sort V. M. Moroz
title Experimental modeling of sudden death pathological mechanisms in Na+ channel blocker treatment
title_short Experimental modeling of sudden death pathological mechanisms in Na+ channel blocker treatment
title_full Experimental modeling of sudden death pathological mechanisms in Na+ channel blocker treatment
title_fullStr Experimental modeling of sudden death pathological mechanisms in Na+ channel blocker treatment
title_full_unstemmed Experimental modeling of sudden death pathological mechanisms in Na+ channel blocker treatment
title_sort experimental modeling of sudden death pathological mechanisms in na+ channel blocker treatment
publisher «FIRMA «SILICEA» LLC 
series Российский кардиологический журнал
issn 1560-4071
2618-7620
publishDate 2006-06-01
description In laboratory rats, a minimal arrhythmogenic dose of 1, 5 % KCl solution (15 mg/kg) was injected intravenously in 2 seconds. Hypopolarization arrhythmias were registered in 3-10 seconds, followed by regular sinus rhythm. In experimental groups, the animals received a minimal arrhythmogenic dose of KCl in 5 minutes after intravenous infusion of 1 % novocainamidum (20 mg/kg) or 0, 25 % ethacyzin (4 mg/kg). In all 20 rats, N a+ cannel blocker and KCl bolus administration resulted in cardioplegy; in every second animal, asystolia and death were registered (40 % and 60 %, respectively). Therefore, in coronary heart disease patients, receiving Na+ channel blockers, sudden death pathogenesis might be influenced by membrane hyperpolarization, due to Na+/K+-ATPase dysfunction, low cytosol concentration of K+ ions, and their decreased flow from the cells in final repolarization phase.
topic sudden death
cardiac arrhythmias
membrane hyperpolarization
hyperkaliemia
arrhythmogenic effects of antiarrhythmics
url https://russjcardiol.elpub.ru/jour/article/view/1842
work_keys_str_mv AT vmmoroz experimentalmodelingofsuddendeathpathologicalmechanismsinnachannelblockertreatment
AT tnlipnitsky experimentalmodelingofsuddendeathpathologicalmechanismsinnachannelblockertreatment
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