Electrophysiological effects of disopyramide phosphate during experimental myocardial ischemia

Levites, Rafael; Anderson, Gary J.

doi:10.1016/0002-8703(79)90046-2

Cited by 13 publications

(4 citation statements)

References 22 publications

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“…Refractory periods have been reported to undergo various changes during myocardial ischaemia, although shortening has been the most common finding (Levites et al, 1975;Downar et al, 1977;Bastford et al, 1978;Levine et al, 1978;Bissett et al, 1979;Levites & Anderson, 1979;Stewart et al, 1980). Failure of the refractory periods to shorten in the face of the universally observed shortening of action potential duration has usually been attributed by previous workers to a state ofpost-repolarisation refractoriness (Lazzara et al, 1978;Bissett et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

A protective effect of sulphinpyrazone against coronary occlusion‐induced shortening of myocardial refractory periods in the rat

Northover

1986

British J Pharmacology

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1 The hearts of anaesthetized, artificially ventilated rats were exposed, and the left coronary artery occluded. The diastolic threshold voltage for stimulation (DTV), the duration of the bipolar electrogram (DBE) and the functional refractory period (FRP) of the ischaemic area were measured at minute intervals for an hour after occlusion. 2 Coronary occlusion caused a rise in DTV, a prolongation of the DBE and a biphasic change in the FRP, with an initial prolongation phase (1-4 min) followed by a decline to below pre-occlusion values (5-15 min). 3 Episodes ofventricular tachyarrhythmia (VT) were most frequent during the period 5-15 min after the onset of occlusion of the coronary artery. This coincided with the period when FRP was minimal and the difference between DBE and FRP was maximal. 4 Pretreatment of rats with sulphinpyrazone (2.5-40mgkg-') or indomethacin (5-20mgkg-') protected against the episodes of coronary occlusion-induced VT and against the associated decline in FRP of the ischaemic muscle. Sulphinpyrazone was more effective than indomethacin in this respect and a combination of the two drugs was approximately as effective as sulphinpyrazone alone. 5 It was concluded that sulphinpyrazone protects rats against coronary occlusion-induced episodes of VT by reducing the risk of ventricular action potential re-entry. This effect is probably due to protection against the ischaemia-induced shortening of the myocardial FRP.

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Section: Discussionmentioning

confidence: 99%

A protective effect of sulphinpyrazone against coronary occlusion‐induced shortening of myocardial refractory periods in the rat

Northover

1986

British J Pharmacology

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“…Arrhythmia was detected and marked, for 10 and 100 μM disopyramide. The most prominent effects of disopyramide were decreased contractility (as suggested by Levites et al, see (Levites & Anderson, 1979)). Furthermore, we observed a reduction in EFP spike amplitude across all cell types.…”

Section: Resultsmentioning

confidence: 70%

“…Disopyramide is part of the high risk category and is an anti-arrhythmic agent that inhibits the fast sodium channel conduction. In addition to that, it has a negative inotropic effect on ventricular myocardium, significantly decreasing the contractility (Levites & Anderson, 1979). In Fig.…”

Section: Resultsmentioning

confidence: 99%

Cross - site comparison of excitation-contraction coupling using impedance and field potential recordings in hiPSC cardiomyocytes

Bot¹,

Juhász

Haeusermann

et al. 2018

Journal of Pharmacological and Toxicological Methods

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“…A major limitation for the wide use of quinidine in the world is its lack of accessibility. 53,54 Viskin et al 54 55 These effects can explain its efficacy in BrS. Even though the effect of disopyramide in slightly augmenting ST elevation in BrS has been described in small studies, it has not been associated with development of premature ventricular complexes or VT/VF.…”

Section: Limited Worldwide Commercial Availability Of the Drugmentioning

confidence: 99%

Pharmacological Therapy in Brugada Syndrome

Brodie

Michowitz

Belhassen

2018

Arrhythmia &Amp; Electrophysiology Review

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Brugada syndrome (BrS) is a cardiac disease caused by an inherited ion channelopathy associated with a propensity to develop ventricular fibrillation. Implantable cardioverter defibrillator implantation is recommended in BrS, based on the clinical presentation in the presence of diagnostic ECG criteria. Implantable cardioverter defibrillator implantation is not always indicated or sufficient in BrS, and is associated with a high device complication rate. Pharmacological therapy aimed at rebalancing the membrane action potential can prevent arrhythmogenesis in BrS. Quinidine, a class 1A antiarrhythmic drug with significant Ito blocking properties, is the most extensively used drug for the prevention of arrhythmias in BrS. The present review provides contemporary data gathered on all drugs effective in the therapy of BrS, and on ineffective or contraindicated antiarrhythmic drugs.

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Electrophysiological effects of disopyramide phosphate during experimental myocardial ischemia

Cited by 13 publications

References 22 publications

A protective effect of sulphinpyrazone against coronary occlusion‐induced shortening of myocardial refractory periods in the rat

A protective effect of sulphinpyrazone against coronary occlusion‐induced shortening of myocardial refractory periods in the rat

Cross - site comparison of excitation-contraction coupling using impedance and field potential recordings in hiPSC cardiomyocytes

Pharmacological Therapy in Brugada Syndrome

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