Rate-dependent effects of sematilide on action potential duration in isolated guinea pig ventricular myocytes.

doi:10.1016/s0022-3565(25)22784-7

Paper

Rate-dependent effects of sematilide on action potential duration in isolated guinea pig ventricular myocytes.

Published Oct 1, 1994 · T. Sawanobori, H. Adaniya, T. Namiki

The Journal of pharmacology and experimental therapeutics

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Abstract

Abstract hidden due to publisher request; this does not indicate any issues with the research. Click the full text link above to read the abstract and view the original source.

In Vitro Study

Study Snapshot

Sematilide prolongs action potential duration in guinea pig ventricular myocytes by blocking the rapidly activating component of the delayed outward K+ current, with a reverse use-dependent effect at 2.5 Hz.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

Paper

Rate-dependent effects of sematilide on action potential duration in isolated guinea pig ventricular myocytes.

References

Citations

Current Practices in Safety Pharmacology

Safety pharmacology studies new and marketed therapeutic agents to identify their pharmacodynamic properties, aiding in understanding human risk posed by drug exposure.

Relationships between preclinical cardiac electrophysiology, clinical QT interval prolongation and torsade de pointes for a broad range of drugs: evidence for a provisional safety margin in drug development.

Most drugs associated with torsade de pointes in humans also cause hERG K(+) channel block at concentrations close to or superimposed upon clinical use, with a 30-fold margin between C(max) and clinical use being a safe range.

Comparison of the in vivo electrophysiological and proarrhythmic effects of amiodarone with those of a selective class III drug, sematilide, using a canine chronic atrioventricular block model.

Amiodarone's IKr channel inhibition and additional ion channel blocking action may contribute to the prevention of torsade de pointes, while sematilide's high dose can cause fatal arrhythmias.

Effects of a Typical IKr Channel Blocker Sematilide on the Relationship Between Ventricular Repolarization, Refractoriness and Onset of Torsades de Pointes

Sematilide prolongs the terminal repolarization process, increasing the risk of conduction slowing at less complete repolarization levels, potentially increasing the incidence of torsades de pointes.

Antiarrhythmic drugs and cardiac ion channels: mechanisms of action.

Antiarrhythmic drugs modify vulnerable parameters in cardiac ion channels and receptors, potentially stopping or preventing arrhythmias by affecting specific channels and receptors.