Variazioni della risposta aritmogena alle catecolamine in corso di ischemia miocardica acuta.

Translated title of the contribution: Variations in arrhythmogenic response to catecholamines in acute myocardial ischemia

S. G. Priori, P. B. Corr

Research output: Contribution to journalArticle

Abstract

Several studies have demonstrated that focal mechanisms contribute to arrhythmogenesis during acute myocardial ischemia in vivo. However, the biochemical derangements during ischemia may either potentiate or depress the electrophysiological mechanisms leading to focal arrhythmias. In the study presented here we have characterized the consequences of various levels of cellular depression and of alterations in the extracellular environment on the development of early (EADs) and delayed (DADs) afterdepolarizations induced by catecholamines. Adult canine myocytes were exposed to: normoxia; hypoxia (pO2 less than 10 mmHg); hypoxia + high K+ or cyanide infusion. Early and delayed afterdepolarizations were induced by alpha or beta adrenergic stimulation in the different experimental conditions by infusing isoproterenol (10(-8)-10(-6) M) or phenylephrine (10(-7)-10(-5) M) + the betablocker nadolol. Hypoxia did not modify EADs or DADs induced by beta stimulation and potentiated DADs induced by alpha stimulation; hypoxia + high K+ blunted DADs induced by both types of stimulation and cyanide infusion completely prevented and suppressed them. Thus, triggered arrhythmias dependent upon adrenergic stimulation can either be potentiated or inhibited by the biochemical derangements of acute ischemia. Focal arrhythmias are more likely to occur in the borderline ischemic cells where cellular depression and extracellular K+ accumulation are less marked.

Original languageItalian
Pages (from-to)229-235
Number of pages7
JournalCardiologia
Volume36
Issue number3
Publication statusPublished - Mar 1991

Fingerprint

Catecholamines
Myocardial Ischemia
Cardiac Arrhythmias
Cyanides
Adrenergic Agents
Ischemia
Nadolol
Phenylephrine
Isoproterenol
Muscle Cells
Canidae
Hypoxia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Variazioni della risposta aritmogena alle catecolamine in corso di ischemia miocardica acuta. / Priori, S. G.; Corr, P. B.

In: Cardiologia, Vol. 36, No. 3, 03.1991, p. 229-235.

Research output: Contribution to journalArticle

@article{5d81ffe497be4f079a81687df5ae7edb,
title = "Variazioni della risposta aritmogena alle catecolamine in corso di ischemia miocardica acuta.",
abstract = "Several studies have demonstrated that focal mechanisms contribute to arrhythmogenesis during acute myocardial ischemia in vivo. However, the biochemical derangements during ischemia may either potentiate or depress the electrophysiological mechanisms leading to focal arrhythmias. In the study presented here we have characterized the consequences of various levels of cellular depression and of alterations in the extracellular environment on the development of early (EADs) and delayed (DADs) afterdepolarizations induced by catecholamines. Adult canine myocytes were exposed to: normoxia; hypoxia (pO2 less than 10 mmHg); hypoxia + high K+ or cyanide infusion. Early and delayed afterdepolarizations were induced by alpha or beta adrenergic stimulation in the different experimental conditions by infusing isoproterenol (10(-8)-10(-6) M) or phenylephrine (10(-7)-10(-5) M) + the betablocker nadolol. Hypoxia did not modify EADs or DADs induced by beta stimulation and potentiated DADs induced by alpha stimulation; hypoxia + high K+ blunted DADs induced by both types of stimulation and cyanide infusion completely prevented and suppressed them. Thus, triggered arrhythmias dependent upon adrenergic stimulation can either be potentiated or inhibited by the biochemical derangements of acute ischemia. Focal arrhythmias are more likely to occur in the borderline ischemic cells where cellular depression and extracellular K+ accumulation are less marked.",
author = "Priori, {S. G.} and Corr, {P. B.}",
year = "1991",
month = "3",
language = "Italian",
volume = "36",
pages = "229--235",
journal = "Cardiologia (Rome, Italy)",
issn = "0393-1978",
publisher = "Societa Italiana di Cardiologia",
number = "3",

}

TY - JOUR

T1 - Variazioni della risposta aritmogena alle catecolamine in corso di ischemia miocardica acuta.

AU - Priori, S. G.

AU - Corr, P. B.

PY - 1991/3

Y1 - 1991/3

N2 - Several studies have demonstrated that focal mechanisms contribute to arrhythmogenesis during acute myocardial ischemia in vivo. However, the biochemical derangements during ischemia may either potentiate or depress the electrophysiological mechanisms leading to focal arrhythmias. In the study presented here we have characterized the consequences of various levels of cellular depression and of alterations in the extracellular environment on the development of early (EADs) and delayed (DADs) afterdepolarizations induced by catecholamines. Adult canine myocytes were exposed to: normoxia; hypoxia (pO2 less than 10 mmHg); hypoxia + high K+ or cyanide infusion. Early and delayed afterdepolarizations were induced by alpha or beta adrenergic stimulation in the different experimental conditions by infusing isoproterenol (10(-8)-10(-6) M) or phenylephrine (10(-7)-10(-5) M) + the betablocker nadolol. Hypoxia did not modify EADs or DADs induced by beta stimulation and potentiated DADs induced by alpha stimulation; hypoxia + high K+ blunted DADs induced by both types of stimulation and cyanide infusion completely prevented and suppressed them. Thus, triggered arrhythmias dependent upon adrenergic stimulation can either be potentiated or inhibited by the biochemical derangements of acute ischemia. Focal arrhythmias are more likely to occur in the borderline ischemic cells where cellular depression and extracellular K+ accumulation are less marked.

AB - Several studies have demonstrated that focal mechanisms contribute to arrhythmogenesis during acute myocardial ischemia in vivo. However, the biochemical derangements during ischemia may either potentiate or depress the electrophysiological mechanisms leading to focal arrhythmias. In the study presented here we have characterized the consequences of various levels of cellular depression and of alterations in the extracellular environment on the development of early (EADs) and delayed (DADs) afterdepolarizations induced by catecholamines. Adult canine myocytes were exposed to: normoxia; hypoxia (pO2 less than 10 mmHg); hypoxia + high K+ or cyanide infusion. Early and delayed afterdepolarizations were induced by alpha or beta adrenergic stimulation in the different experimental conditions by infusing isoproterenol (10(-8)-10(-6) M) or phenylephrine (10(-7)-10(-5) M) + the betablocker nadolol. Hypoxia did not modify EADs or DADs induced by beta stimulation and potentiated DADs induced by alpha stimulation; hypoxia + high K+ blunted DADs induced by both types of stimulation and cyanide infusion completely prevented and suppressed them. Thus, triggered arrhythmias dependent upon adrenergic stimulation can either be potentiated or inhibited by the biochemical derangements of acute ischemia. Focal arrhythmias are more likely to occur in the borderline ischemic cells where cellular depression and extracellular K+ accumulation are less marked.

UR - http://www.scopus.com/inward/record.url?scp=0026131150&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026131150&partnerID=8YFLogxK

M3 - Articolo

C2 - 1913717

AN - SCOPUS:0026131150

VL - 36

SP - 229

EP - 235

JO - Cardiologia (Rome, Italy)

JF - Cardiologia (Rome, Italy)

SN - 0393-1978

IS - 3

ER -