Effects of halothane on action potential configuration in sub-endocardial and sub-epicardial myocytes from normotensive and hypertensive rat left ventricle

Rithalia, A; Hopkins, Philip M.; Harrison, Simon

doi:10.1093/bja/aeg093

Cited by 5 publications

(4 citation statements)

References 10 publications

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“…The selective lengthening of the SHR, EPI, APD is particularly interesting as a similar effect has been reported in hypertrophy induced by isoprenaline [13] and by exercise [11], thus lengthening of EPI, APD may be a common response in hypertrophic models of the rat. A likely candidate for the lengthening of the EPI APD is a reduced density of the transient outward K + current, I to ( [13,22], but see [32]). Altered [Ca 2 + ]i characteristics may also influence the transmural changes in electrical activity via effects upon Ca 2 + activated currents and stress -strain (stretch) relationships.…”

Section: Contraction [Ca 2+ ]I and Apdmentioning

confidence: 99%

Transmural changes in size, contractile and electrical properties of SHR left ventricular myocytes during compensated hypertrophy

McCrossan

2004

Cardiovascular Research

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Our findings show that in the SHR, the effect of hypertension upon the morphology, mechanical activity and electrical activity of left ventricular myocytes is dependent upon their transmural location. Therefore, in addition to the overall compensating response to hypertension, i.e. increased contractility, there are likely to be regionally specific alterations in mechano-electric interactions that may influence the properties of this important model, e.g. its pre-disposition to arrhythmia whilst still in a compensated state.

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Section: Contraction [Ca 2+ ]I and Apdmentioning

confidence: 99%

Transmural changes in size, contractile and electrical properties of SHR left ventricular myocytes during compensated hypertrophy

McCrossan

2004

Cardiovascular Research

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“…Several reports have been conducted on differences in cardiomyocyte electrophysiology in left ventricular hypertrophy models compared to non-left ventricular hypertrophy models. 6,[28][29][30][31][32] Electrophysiologic changes accompanied with left ventricular hypertrophy or heart failure in animal models include prolonged action potential durations, [32][33][34] altered sodium ion currents, 29 increased sodium ion/calcium ion exchanger currents, and decreased calcium ion currents. 6,28 Changes in sodium ion current density were inconsistent among the previous reports.…”

Section: In Vitro Experimentsmentioning

confidence: 99%

Left Ventricular Hypertrophy Increases Susceptibility to Bupivacaine-induced Cardiotoxicity through Overexpression of Transient Receptor Potential Canonical Channels in Rats

Hino¹,

Matsuura²,

Kuno³

et al. 2020

Anesthesiology

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Background Local anesthetics, particularly potent long acting ones such as bupivacaine, can cause cardiotoxicity by inhibiting sodium ion channels; however, the impact of left ventricular hypertrophy on the cardiotoxicity and the underlying mechanisms remain undetermined. Transient receptor potential canonical (TRPC) channels are upregulated in left ventricular hypertrophy. Some transient receptor potential channel subtypes have been reported to pass relatively large cations, including protonated local anesthetics; this is known as the “pore phenomenon.” The authors hypothesized that bupivacaine-induced cardiotoxicity is more severe in left ventricular hypertrophy due to upregulated TRPC channels. Methods The authors used a modified transverse aortic constriction model as a left ventricular hypertrophy. Cardiotoxicity caused by bupivacaine was compared between sham and aortic constriction male rats, and the underlying mechanisms were investigated by recording sodium ion channel currents and immunocytochemistry of TRPC protein in cardiomyocytes. Results The time to cardiac arrest by bupivacaine was shorter in aortic constriction rats (n =11) than in sham rats (n = 12) (mean ± SD, 1,302 ± 324 s vs. 1,034 ± 211 s; P = 0.030), regardless of its lower plasma concentration. The half-maximal inhibitory concentrations of bupivacaine toward sodium ion currents were 4.5 and 4.3 μM, which decreased to 3.9 and 2.6 μM in sham and aortic constriction rats, respectively, upon coapplication of 1-oleoyl-2-acetyl-sn-glycerol, a TRPC3 channel activator. In both groups, sodium ion currents were unaffected by QX-314, a positively charged lidocaine derivative, that hardly permeates the cell membrane, but was significantly decreased with QX-314 and 1-oleoyl-2-acetyl-sn-glycerol coapplication (sham: 79 ± 10% of control; P = 0.004; aortic constriction: 47± 27% of control; P = 0.020; n = 5 cells per group). Effects of 1-oleoyl-2-acetyl-sn-glycerol were antagonized by a specific TRPC3 channel inhibitor. Conclusions Left ventricular hypertrophy exacerbated bupivacaine-induced cardiotoxicity, which could be a consequence of the “pore phenomenon” of TRPC3 channels upregulated in left ventricular hypertrophy. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That New

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“…The basic characteristic in LVH on the microscopic scale is the increase in size of individual cardiomyocytes documented in numerous animal and human studies. Additionally, the hypertrophied cardiomyocytes differ from the normal cardiomyocytes not only in diameter and length but also in branching and number of connected cardiomyocytes [18][19][20][21]. These structural changes affect upstroke velocity of the action potential, the action potential propagation, conduction velocity, and cell-to-cell impulse propagation [22][23][24].…”

Section: Left Ventricular Hypertrophymentioning

confidence: 99%

Missing Link Between Molecular Aspects of Ventricular Arrhythmias and QRS Complex Morphology in Left Ventricular Hypertrophy

Bachárová

2019

IJMS

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The aim of this opinion paper is to point out the knowledge gap between evidence on the molecular level and clinical diagnostic possibilities in left ventricular hypertrophy (LVH) regarding the prediction of ventricular arrhythmias and monitoring the effect of therapy. LVH is defined as an increase in left ventricular size and is associated with increased occurrence of ventricular arrhythmia. Hypertrophic rebuilding of myocardium comprises interrelated processes on molecular, subcellular, cellular, tissue, and organ levels affecting electrogenesis, creating a substrate for triggering and maintaining arrhythmias. The knowledge of these processes serves as a basis for developing targeted therapy to prevent and treat arrhythmias. In the clinical practice, the method for recording electrical phenomena of the heart is electrocardiography. The recognized clinical electrocardiogram (ECG) predictors of ventricular arrhythmias are related to alterations in electrical impulse propagation, such as QRS complex duration, QT interval, early repolarization, late potentials, and fragmented QRS, and they are not specific for LVH. However, the simulation studies have shown that the QRS complex patterns documented in patients with LVH are also conditioned remarkably by the alterations in impulse propagation. These QRS complex patterns in LVH could be potentially recognized for predicting ventricular arrhythmia and for monitoring the effect of therapy.

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Effects of halothane on action potential configuration in sub-endocardial and sub-epicardial myocytes from normotensive and hypertensive rat left ventricle

Cited by 5 publications

References 10 publications

Transmural changes in size, contractile and electrical properties of SHR left ventricular myocytes during compensated hypertrophy

Transmural changes in size, contractile and electrical properties of SHR left ventricular myocytes during compensated hypertrophy

Left Ventricular Hypertrophy Increases Susceptibility to Bupivacaine-induced Cardiotoxicity through Overexpression of Transient Receptor Potential Canonical Channels in Rats

Missing Link Between Molecular Aspects of Ventricular Arrhythmias and QRS Complex Morphology in Left Ventricular Hypertrophy

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