Regional electrophysiological effects of left ventricular hypertrophy in isolated rabbit hearts under normal and ischaemic conditions

R Wolk, K P Sneddon, J Dempster, K A Kane, S M Cobbe, M N Hicks

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Left ventricular hypertrophy (LVH) has been reported to produce differential electrophysiological effects in isolated epicardial and endocardial cells. This study aimed to examine regional electrophysiological effects of LVH in normal and ischaemic conditions in the whole heart.
LVH was secondary to perinephritis-induced hypertension. Monophasic action potential duration (MAPD(90)), effective refractory period (ERP) and conduction delay were measured in paced, isolated working rabbit hearts either at one right ventricular and two left ventricular sites (apical and basal epicardium) or at three left ventricular sites (apical and basal epicardium, apical: endocardium). The hearts were subjected to 30 min of regional ischaemia and 15 min of reperfusion.
In non-ischaemic conditions, LVH produced uniform prolongation of MAPD(90) and ERP in the left ventricular epicardium, but not in the endocardium. After coronary artery occlusion, LVH significantly increased ischaemia-induced transepicardial dispersion of repolarisation, but not refractoriness. LVH did not affect arrhythmogenesis in either non-ischaemic or ischaemic conditions.
Differential effects of LVH on epicardial and endocardial electrophysiological parameters are also observed in the whole heart. In addition, the sensitivity of hypertrophied myocardium to ischaemia is increased and leads to an increase in ischaemia-induced dispersion of repolarisation. However, neither dispersion of refractoriness nor arrhythmogenesis are affected by LVH in non-ischaemic or ischaemic conditions in this experimental model.
LanguageEnglish
Pages120-128
Number of pages9
JournalCardiovascular Research
Volume48
Issue number1
DOIs
Publication statusPublished - Oct 2000

Fingerprint

Left Ventricular Hypertrophy
Rabbits
Pericardium
Ischemia
Endocardium
Perinephritis
Coronary Occlusion
Action Potentials
Reperfusion
Coronary Vessels
Myocardium
Theoretical Models
Hypertension

Keywords

  • action potentials
  • analysis of variance
  • animals
  • endocardium
  • heart
  • left ventricular hypertrophy
  • male
  • myocardial Ischemia
  • myocardial reperfusion
  • pericardium
  • rabbits

Cite this

Wolk, R ; Sneddon, K P ; Dempster, J ; Kane, K A ; Cobbe, S M ; Hicks, M N. / Regional electrophysiological effects of left ventricular hypertrophy in isolated rabbit hearts under normal and ischaemic conditions. In: Cardiovascular Research. 2000 ; Vol. 48, No. 1. pp. 120-128.
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Regional electrophysiological effects of left ventricular hypertrophy in isolated rabbit hearts under normal and ischaemic conditions. / Wolk, R; Sneddon, K P; Dempster, J; Kane, K A; Cobbe, S M; Hicks, M N.

In: Cardiovascular Research, Vol. 48, No. 1, 10.2000, p. 120-128.

Research output: Contribution to journalArticle

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T1 - Regional electrophysiological effects of left ventricular hypertrophy in isolated rabbit hearts under normal and ischaemic conditions

AU - Wolk, R

AU - Sneddon, K P

AU - Dempster, J

AU - Kane, K A

AU - Cobbe, S M

AU - Hicks, M N

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N2 - Left ventricular hypertrophy (LVH) has been reported to produce differential electrophysiological effects in isolated epicardial and endocardial cells. This study aimed to examine regional electrophysiological effects of LVH in normal and ischaemic conditions in the whole heart. LVH was secondary to perinephritis-induced hypertension. Monophasic action potential duration (MAPD(90)), effective refractory period (ERP) and conduction delay were measured in paced, isolated working rabbit hearts either at one right ventricular and two left ventricular sites (apical and basal epicardium) or at three left ventricular sites (apical and basal epicardium, apical: endocardium). The hearts were subjected to 30 min of regional ischaemia and 15 min of reperfusion. In non-ischaemic conditions, LVH produced uniform prolongation of MAPD(90) and ERP in the left ventricular epicardium, but not in the endocardium. After coronary artery occlusion, LVH significantly increased ischaemia-induced transepicardial dispersion of repolarisation, but not refractoriness. LVH did not affect arrhythmogenesis in either non-ischaemic or ischaemic conditions. Differential effects of LVH on epicardial and endocardial electrophysiological parameters are also observed in the whole heart. In addition, the sensitivity of hypertrophied myocardium to ischaemia is increased and leads to an increase in ischaemia-induced dispersion of repolarisation. However, neither dispersion of refractoriness nor arrhythmogenesis are affected by LVH in non-ischaemic or ischaemic conditions in this experimental model.

AB - Left ventricular hypertrophy (LVH) has been reported to produce differential electrophysiological effects in isolated epicardial and endocardial cells. This study aimed to examine regional electrophysiological effects of LVH in normal and ischaemic conditions in the whole heart. LVH was secondary to perinephritis-induced hypertension. Monophasic action potential duration (MAPD(90)), effective refractory period (ERP) and conduction delay were measured in paced, isolated working rabbit hearts either at one right ventricular and two left ventricular sites (apical and basal epicardium) or at three left ventricular sites (apical and basal epicardium, apical: endocardium). The hearts were subjected to 30 min of regional ischaemia and 15 min of reperfusion. In non-ischaemic conditions, LVH produced uniform prolongation of MAPD(90) and ERP in the left ventricular epicardium, but not in the endocardium. After coronary artery occlusion, LVH significantly increased ischaemia-induced transepicardial dispersion of repolarisation, but not refractoriness. LVH did not affect arrhythmogenesis in either non-ischaemic or ischaemic conditions. Differential effects of LVH on epicardial and endocardial electrophysiological parameters are also observed in the whole heart. In addition, the sensitivity of hypertrophied myocardium to ischaemia is increased and leads to an increase in ischaemia-induced dispersion of repolarisation. However, neither dispersion of refractoriness nor arrhythmogenesis are affected by LVH in non-ischaemic or ischaemic conditions in this experimental model.

KW - action potentials

KW - analysis of variance

KW - animals

KW - endocardium

KW - heart

KW - left ventricular hypertrophy

KW - male

KW - myocardial Ischemia

KW - myocardial reperfusion

KW - pericardium

KW - rabbits

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DO - 10.1016/S0008-6363(00)00149-8

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EP - 128

JO - Cardiovascular Research

T2 - Cardiovascular Research

JF - Cardiovascular Research

SN - 0008-6363

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ER -