Halothane Inhibits Contraction and Action Potential Duration to a Greater Extent in Subendocardial than Subepicardial Myocytes from the Rat Left Ventricle

Rithalia, A; Gibson, Clare N.; Hopkins, Philip M.; Harrison, Simon

doi:10.1097/00000542-200111000-00027

Cited by 9 publications

(5 citation statements)

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“…This could increase the susceptibility of the heart to arrhythmias initially induced by premature ventricular excitation through physiological phenomena such as EADs and triggered beats or via artificial premature excitation using PES. This first report of such phenomena in the isolated, perfused whole-heart model complements one previous study in isolated endocardial and epicardial rat myocytes that suggested that a reduction in TDR might also be proarrhythmic (Rithalia et al 2001). Our results in the intact myocardium directly demonstrate that a reduced transmural gradient in APD can afford a mechanism of proarrhythmia.…”

Section: Discussionsupporting

confidence: 84%

“…This in turn would facilitate the generation of local conduction block and of consequent re‐entrant arrhythmogenesis (Wolk et al. 1999, Rithalia et al. 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Although a reduction in TDR is generally considered to reduce rather than increase the likelihood of arrhythmogenesis, one potential outcome of altered myocardial repolarization gradients would be an increased probability of repolarization gradient collision. This in turn would facilitate the generation of local conduction block and of consequent re-entrant arrhythmogenesis (Wolk et al 1999, Rithalia et al 2001. This could increase the susceptibility of the heart to arrhythmias initially induced by premature ventricular excitation through physiological phenomena such as EADs and triggered beats or via artificial premature excitation using PES.…”

Section: Discussionmentioning

confidence: 99%

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Arrhythmogenic mechanisms in the isolated perfused hypokalaemic murine heart

et al. 2007

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] o respectively. Endocardial APD 90 s correspondingly increased from 51.6 AE 1.9 ms (n ¼ 7) to 62.8 AE 2.8 ms (n ¼ 7) and 62.9 AE 5.9 ms (n ¼ 11) giving reductions in endocardial-epicardial differences, DAPD 90 , from 14.4 AE 2.6 to 4.4 AE 5.0 and )3.4 AE 6.0 ms respectively. Early afterdepolarizations (EADs) occurred in epicardia in three of seven spontaneously beating hearts at 4 mm [K + ] o with triggered beats followed by episodes of non-sustained VT in nine of 11 preparations at 3 mm. Programmed electrical stimulation never induced arrhythmic events in preparations perfused with normokalemic solutions yet induced VT in two of seven and nine of 11 preparations at 4 and 3 mm

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Section: Discussionsupporting

confidence: 84%

“…This in turn would facilitate the generation of local conduction block and of consequent re‐entrant arrhythmogenesis (Wolk et al. 1999, Rithalia et al. 2001).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Arrhythmogenic mechanisms in the isolated perfused hypokalaemic murine heart

et al. 2007

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“…Several volatile anesthetics have been reported to affect the APD (11)(12)(13). However, the effects have been extremely inhomogeneous.…”

Section: Basic Electrophysiology Of the Cardiomyocyte And Arrhythmiasmentioning

confidence: 99%

Effects of volatile anesthetics on cardiac ion channels

Hüneke¹,

Fassl²,

Rossaint³

et al. 2004

Acta Anaesthesiol Scand

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The focus of the present review is on how interference with various ion channels in the heart may be the molecular basis for cardiac side-effects of gaseous anesthetics. Electrophysiological studies in isolated animal and human cardiomyocytes have identified the L-type Ca(2+) channel as a prominent target of anesthetics. Since this ion channel is of fundamental importance for the plateau phase of the cardiac action potential as well as for Ca(2+)-mediated electromechanical coupling, its inhibition may facilitate arrhythmias by shortening the refractory period and may decrease the contractile force. Effective inhibition of this ion channel has been shown for clinically used concentrations of halothane and, to a lesser extent, of isoflurane and sevoflurane, whereas xenon was without effect. Anesthetics furthermore inhibit several types of voltage-gated K(+) channels. Thereby, they may disturb the repolarization and bear a considerable risk for the induction of ventricular tachycardia in predisposed patients. In future, an advanced understanding of cardiac side-effects of anesthetics will derive from more detailed analyses of how and which channels are affected as well as from a better comprehension of how altered channel function influences heart function.

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“…Even responses to physiologic (exercise, 14 memory 15 ), pharmacologic (drugs 16 ), and pathophysiologic stimuli (disease) vary in the endocardium versus the epicardium. In some instances, responses to drugs and disease 17 have been shown to attenuate baseline heterogeneities.…”

Section: Introductionmentioning

confidence: 99%