Expressed monophasic action potential alternans before the onset of ventricular arrhythmias induced by intracoronary bolus administration of endothelin-1 in dogs

B. Merkely, Hajnalka Vágó, Orsolya Kiss, E. Zima, Gábor Szucs, L. Gellér, A. Juhász-Nagy

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Abstract

We showed previously a direct arrhythmogenic effect of the intracoronary infusion of endothelin-1 (ET-1). We aimed to examine the electrophysiological effects of intracoronary bolus administration of ET-1 using monophasic action potential (MAP) recordings. Eight mongrel dogs received boli of ET-1 (1 and 2 nmol) into the left anterior descending coronary artery. These intracoronary ET-1 boli rapidly caused a marked decrease in coronary blood flow (1 nmol, 78±7%; 2 nmol, 89±7%). Ischaemic changes of MAP morphology, a decrease in upstroke velocity (baseline, 1.78±0.2 V/s; 1 nmol, 0.95±0.18 V/s; 2 nmol, 0.45±0.21 V/s; P <0.01) and a decrease in MAP duration at 90% repolarization (MAPD90) [1 nmol, from 191±3 to 176±5 ms (P <0.05); 2 nmol, from 212±4 to 180±8 ms (P <0.05)] occurred after ET-1 bolus administration. However, at 7-10 min after the 1 nmol bolus, a significant increase in MAPD90 was observed (10 min, in the left ventricular anterior epicardial region: from 191±3 to 206±6 ms; P <0.05). The incidence of ventricular arrhythmias was as follows: after the 1 nmol ET-1 bolus: ventricular tachycardia, 3/8 animals; ventricular fibrillation, 1/8; after the 2nmol ET-1 bolus: ventricular tachycardia, 5/7; ventricular fibrillation, 5/7. MAP alternans was present in each animal (1 nmol, 18.2±5.8%; 2 nmol, 10.8±2.5%). Thus electrophysiological and coronary blood flow changes indicate the predominance of an ischaemic arrhythmogenic effect of the bolus administration of ET-1 (shortening of action potential duration; appearance of MAP alternans), whereas the observed delayed prolongation of MAPD90 suggests a direct arrhythmogenic effect of ET-1. The expressed MAP alternans could have a pathogenic role in the onset of ventricular arrhythmias induced by an intracoronary bolus of ET-1.

Original languageEnglish
JournalClinical Science
Volume103
Issue numberSUPPL. 48
Publication statusPublished - Aug 2002

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Endothelin-1
Action Potentials
Cardiac Arrhythmias
Dogs
Ventricular Fibrillation
Ventricular Tachycardia
Coronary Vessels
Incidence

Keywords

  • Cardiac electrophysiology
  • Monophasic action potential
  • Ventricular arrhythmia

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{9af8f0efaa724e15a7e94718dde7772d,
title = "Expressed monophasic action potential alternans before the onset of ventricular arrhythmias induced by intracoronary bolus administration of endothelin-1 in dogs",
abstract = "We showed previously a direct arrhythmogenic effect of the intracoronary infusion of endothelin-1 (ET-1). We aimed to examine the electrophysiological effects of intracoronary bolus administration of ET-1 using monophasic action potential (MAP) recordings. Eight mongrel dogs received boli of ET-1 (1 and 2 nmol) into the left anterior descending coronary artery. These intracoronary ET-1 boli rapidly caused a marked decrease in coronary blood flow (1 nmol, 78±7{\%}; 2 nmol, 89±7{\%}). Ischaemic changes of MAP morphology, a decrease in upstroke velocity (baseline, 1.78±0.2 V/s; 1 nmol, 0.95±0.18 V/s; 2 nmol, 0.45±0.21 V/s; P <0.01) and a decrease in MAP duration at 90{\%} repolarization (MAPD90) [1 nmol, from 191±3 to 176±5 ms (P <0.05); 2 nmol, from 212±4 to 180±8 ms (P <0.05)] occurred after ET-1 bolus administration. However, at 7-10 min after the 1 nmol bolus, a significant increase in MAPD90 was observed (10 min, in the left ventricular anterior epicardial region: from 191±3 to 206±6 ms; P <0.05). The incidence of ventricular arrhythmias was as follows: after the 1 nmol ET-1 bolus: ventricular tachycardia, 3/8 animals; ventricular fibrillation, 1/8; after the 2nmol ET-1 bolus: ventricular tachycardia, 5/7; ventricular fibrillation, 5/7. MAP alternans was present in each animal (1 nmol, 18.2±5.8{\%}; 2 nmol, 10.8±2.5{\%}). Thus electrophysiological and coronary blood flow changes indicate the predominance of an ischaemic arrhythmogenic effect of the bolus administration of ET-1 (shortening of action potential duration; appearance of MAP alternans), whereas the observed delayed prolongation of MAPD90 suggests a direct arrhythmogenic effect of ET-1. The expressed MAP alternans could have a pathogenic role in the onset of ventricular arrhythmias induced by an intracoronary bolus of ET-1.",
keywords = "Cardiac electrophysiology, Monophasic action potential, Ventricular arrhythmia",
author = "B. Merkely and Hajnalka V{\'a}g{\'o} and Orsolya Kiss and E. Zima and G{\'a}bor Szucs and L. Gell{\'e}r and A. Juh{\'a}sz-Nagy",
year = "2002",
month = "8",
language = "English",
volume = "103",
journal = "Clinical Science",
issn = "0143-5221",
publisher = "Portland Press Ltd.",
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TY - JOUR

T1 - Expressed monophasic action potential alternans before the onset of ventricular arrhythmias induced by intracoronary bolus administration of endothelin-1 in dogs

AU - Merkely, B.

AU - Vágó, Hajnalka

AU - Kiss, Orsolya

AU - Zima, E.

AU - Szucs, Gábor

AU - Gellér, L.

AU - Juhász-Nagy, A.

PY - 2002/8

Y1 - 2002/8

N2 - We showed previously a direct arrhythmogenic effect of the intracoronary infusion of endothelin-1 (ET-1). We aimed to examine the electrophysiological effects of intracoronary bolus administration of ET-1 using monophasic action potential (MAP) recordings. Eight mongrel dogs received boli of ET-1 (1 and 2 nmol) into the left anterior descending coronary artery. These intracoronary ET-1 boli rapidly caused a marked decrease in coronary blood flow (1 nmol, 78±7%; 2 nmol, 89±7%). Ischaemic changes of MAP morphology, a decrease in upstroke velocity (baseline, 1.78±0.2 V/s; 1 nmol, 0.95±0.18 V/s; 2 nmol, 0.45±0.21 V/s; P <0.01) and a decrease in MAP duration at 90% repolarization (MAPD90) [1 nmol, from 191±3 to 176±5 ms (P <0.05); 2 nmol, from 212±4 to 180±8 ms (P <0.05)] occurred after ET-1 bolus administration. However, at 7-10 min after the 1 nmol bolus, a significant increase in MAPD90 was observed (10 min, in the left ventricular anterior epicardial region: from 191±3 to 206±6 ms; P <0.05). The incidence of ventricular arrhythmias was as follows: after the 1 nmol ET-1 bolus: ventricular tachycardia, 3/8 animals; ventricular fibrillation, 1/8; after the 2nmol ET-1 bolus: ventricular tachycardia, 5/7; ventricular fibrillation, 5/7. MAP alternans was present in each animal (1 nmol, 18.2±5.8%; 2 nmol, 10.8±2.5%). Thus electrophysiological and coronary blood flow changes indicate the predominance of an ischaemic arrhythmogenic effect of the bolus administration of ET-1 (shortening of action potential duration; appearance of MAP alternans), whereas the observed delayed prolongation of MAPD90 suggests a direct arrhythmogenic effect of ET-1. The expressed MAP alternans could have a pathogenic role in the onset of ventricular arrhythmias induced by an intracoronary bolus of ET-1.

AB - We showed previously a direct arrhythmogenic effect of the intracoronary infusion of endothelin-1 (ET-1). We aimed to examine the electrophysiological effects of intracoronary bolus administration of ET-1 using monophasic action potential (MAP) recordings. Eight mongrel dogs received boli of ET-1 (1 and 2 nmol) into the left anterior descending coronary artery. These intracoronary ET-1 boli rapidly caused a marked decrease in coronary blood flow (1 nmol, 78±7%; 2 nmol, 89±7%). Ischaemic changes of MAP morphology, a decrease in upstroke velocity (baseline, 1.78±0.2 V/s; 1 nmol, 0.95±0.18 V/s; 2 nmol, 0.45±0.21 V/s; P <0.01) and a decrease in MAP duration at 90% repolarization (MAPD90) [1 nmol, from 191±3 to 176±5 ms (P <0.05); 2 nmol, from 212±4 to 180±8 ms (P <0.05)] occurred after ET-1 bolus administration. However, at 7-10 min after the 1 nmol bolus, a significant increase in MAPD90 was observed (10 min, in the left ventricular anterior epicardial region: from 191±3 to 206±6 ms; P <0.05). The incidence of ventricular arrhythmias was as follows: after the 1 nmol ET-1 bolus: ventricular tachycardia, 3/8 animals; ventricular fibrillation, 1/8; after the 2nmol ET-1 bolus: ventricular tachycardia, 5/7; ventricular fibrillation, 5/7. MAP alternans was present in each animal (1 nmol, 18.2±5.8%; 2 nmol, 10.8±2.5%). Thus electrophysiological and coronary blood flow changes indicate the predominance of an ischaemic arrhythmogenic effect of the bolus administration of ET-1 (shortening of action potential duration; appearance of MAP alternans), whereas the observed delayed prolongation of MAPD90 suggests a direct arrhythmogenic effect of ET-1. The expressed MAP alternans could have a pathogenic role in the onset of ventricular arrhythmias induced by an intracoronary bolus of ET-1.

KW - Cardiac electrophysiology

KW - Monophasic action potential

KW - Ventricular arrhythmia

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