Effects of Acute Global Low-Flow Ischemia on Triggered Arrhythmias in d-Sotalol-Induced Long Q-T Intervals in Perfused Rabbit Hearts

Jf, Spear; En, Moore

doi:10.1097/00005344-200102000-00007

Cited by 3 publications

(1 citation statement)

References 31 publications

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“…I Kr blocker d-sotalol is widely used to establish animal models for LQT2 (Shimizu et al 2000;Liu et al 2005). However, effects of this agent on gap junctions have not been documented (Daleau 1998;Spear et al 2001). The present study provided evidence that gap junction may also contribute to TDR and, thereby, play a role in arrhythmogenesis in LQT2.…”

Section: Arrhythmogenesis In Lqt2mentioning

confidence: 99%

Pharmacological Enhancement of Cardiac Gap Junction Coupling Prevents Arrhythmias in Canine LQT2 Model

Quan

Bai

et al. 2009

Cell Communication & Adhesion

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Gap junctions contribute to the transmural heterogeneity of repolarization in the normal heart and under conditions of prolonged QT interval in the diseased heart. This study examined whether enhancing of gap junction coupling can reduce transmural dispersion of repolarization (TDR) and prevent torsade de pointes (TdP) in a canine LQT2 model. Canine left ventricular wedge preparations were perfused with delayed rectifier potassium current (I Kr ) blocker d-sotalol to mimic LQT2 and the antiarrhythmic peptide 10 (AAP10) was used as a gap junction coupling enhancer. As compared with the control group, the LQT2 group had significantly augmented TDR and higher incidence of TdP associated with increased nonphosphorylated connexin 43 (Cx43). AAP10 prevented augmentation of TDR and induction of TdP while rescuing Cx43 phosphorylation. There was no significant change in the quantity and spatial distribution of Cx43. These data indicate that gap junction enhancer AAP10 can prevent augmentation of TDR and suppress TdP by preventing dephosphorylation of Cx43 in a LQT2 model.

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Section: Arrhythmogenesis In Lqt2mentioning

confidence: 99%

Pharmacological Enhancement of Cardiac Gap Junction Coupling Prevents Arrhythmias in Canine LQT2 Model

Quan

Bai

et al. 2009

Cell Communication & Adhesion

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Effect of lidocaine and amiodarone on transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia

You

Liu

et al. 2005

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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To study the effect of of lidocaine and amiodarone on the transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia and to explore the mechanisms underlying the antiarrhythmic activity of lidocaine and amiodarone, rabbits were randomly divided into 4 groups: control group, ischemia group, lidocaine group and amiodarone group. By the monophasic action potential (MAP) recording technique, MAPs of epicardium, mid-myocardium and endocardium were simultaneously recorded across the left ventricular free wall in rabbit hearts perfused by low-flow ischemia (2.5 mL/min) in Langendorff method to study the transmural dispersion of repolarization (TDR) and arrhythmic induced by ischemia. Our results showed that TDR of three myocardial layers in ischemia group were significantly lengthened after ischemia. TDR was increased from 17.5 +/- 3.9 ms to 31.2 +/- 4.6 ms at the time that concided with the onset of sustained ventricle arrhythmic. Amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia, and no significant difference was found at other ischemia time points. 5 cases had ventriclar arrhythmia in ischemia group (62.5%), but no case in lidocaine group (P < 0.01) and only 1 case in amiodarone group had ventrilar arrhythmia (P < 0.01). No significant difference was found between amiodarone group and lidocaine group. It is concluded that TDR of of three myocardial layers increases significantly at ischemia and it is closely associated with development of ventricular arrhythmia, and amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia and has no effects at other ischemia time points.

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Preconditioning Attenuates the Shortening of Recovery During Coronary Occlusion in Isolated Rabbit Hearts With d-Sotalol-Induced Long QT Intervals

Spear

Moore²

2002

Journal of Cardiovascular Pharmacology

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The effects of 20-min ligations of the anterior branch of the left coronary artery were studied in Langendorff-perfused rabbit hearts with 92 microM D-sotalol added to the perfusate to induce long QT intervals and triggered arrhythmias. Epicardial electrograms, a left ventricular endocardial monophasic action potential, and simulated X and Y lead electrocardiograms were used to characterize ventricular conduction and recovery. In contrast to previous work showing that global ischemia eliminated triggered activity, coronary occlusion did not alter its mean incidence. Although the anatomic distribution of earliest sites of epicardial activation by triggered beats was altered, triggered beats still appeared on the epicardial surface in the nonperfused regions. Coronary occlusion had a small and variable effect on epicardial conduction velocity but caused a significantly greater percent shortening of epicardial activation-recovery intervals in the nonperfused region of hearts given D-sotalol than in control hearts. In hearts given D-sotalol, preconditioning significantly attenuated the shortening of epicardial activation-recovery intervals in response to coronary occlusion. However, preconditioning had no effect on the mean incidence of triggered activity during coronary occlusion. Thus, the persistence of triggered activity and the shortened myocardial recovery time associated with coronary occlusion could contribute to increasing the likelihood of occurrence of malignant ventricular arrhythmias. Preconditioning by attenuating the shortening of recovery would be anti-arrhythmic.

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Effects of Acute Global Low-Flow Ischemia on Triggered Arrhythmias in d-Sotalol-Induced Long Q-T Intervals in Perfused Rabbit Hearts

Cited by 3 publications

References 31 publications

Pharmacological Enhancement of Cardiac Gap Junction Coupling Prevents Arrhythmias in Canine LQT2 Model

Pharmacological Enhancement of Cardiac Gap Junction Coupling Prevents Arrhythmias in Canine LQT2 Model

Effect of lidocaine and amiodarone on transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia

Preconditioning Attenuates the Shortening of Recovery During Coronary Occlusion in Isolated Rabbit Hearts With d-Sotalol-Induced Long QT Intervals

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