What question did this study set out to answer?

The study aimed to compare the effects of new class III antiarrhythmic agents on the delayed K+ rectifier current in guinea pig ventricular myocytes.

November 1, 1992Cardiovascular Research

Differential effects of the new class III antiarrhythmic agents almokalant, E-4031 and D-sotalol, and of quinidine, on delayed rectifier currents in guinea pig ventricular myocytes

Q: What is the clinical evidence from this study?

Study design: Other. Population: Guinea pig ventricular myocytes. Intervention: Almokalant, E-4031, d-sotalol, and quinidine vs. Control experiments. Primary outcome: Delayed K+ rectifier current IK and tail current Itail.

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Key result

Almokalant and E-4031 prominently inhibited the rapidly activating inwardly rectifying component of the delayed K+ rectifier current in guinea pig ventricular myocytes, compared to d-sotalol and quinidine.

Population

Ventricular myocytes from guinea pig hearts

Comparison

Almokalant, E-4031, d-sotalol, and quinidine vs Control experiments

Design

Preclinical

Authors

EWErich WettwerWest German Heart and Vascular Center Essen MGM. GrundkeUniversity of Duisburg-Essen URUrsula RavensElectrophysiology

Discussion

Member takes

Implication

Supports IKr blocker development in preclinical models; leaves open translation to human arrhythmias.

Key Points

The study aimed to compare the effects of new class III antiarrhythmic agents on the delayed K+ rectifier current in guinea pig ventricular myocytes.
Ventricular myocytes from guinea pigs were used.
Whole cell voltage clamp technique measured membrane currents.
IK was activated with step potentials, and the tail current Itail was measured.
D-sotalol significantly decreased IK at 10(-4) M under specific conditions.
Almokalant, E-4031, and quinidine also significantly reduced Itail at varying concentrations (10(-6) M to 10(-5) M).
Inhibition of IK was more prominent with almokalant and E-4031 than with d-sotalol and quinidine.

Structured PICO

Population

Ventricular myocytes from guinea pig hearts

Intervention

Almokalant (10^-6 to 3x10^-6 M), E-4031 (10^-7 to 10^-6 M), d-sotalol (10^-4 M), and quinidine (10^-5 M)

Comparator

Control experiments (spontaneous decline/'run down')

Outcome

Delayed K+ rectifier current IK and tail current Itail measured via whole cell voltage clamp techniquesurrogate

Almokalant and E-4031 prominently inhibit the rapidly activating inwardly rectifying component of the delayed rectifier K+ current in guinea pig ventricular myocytes, which likely contributes to their antiarrhythmic properties.

Cite This Study

Wettwer et al. (1992) studied Guinea pig ventricular myocytes. Almokalant, E-4031, d-sotalol, and quinidine vs. Control experiments was evaluated on Delayed K+ rectifier current IK and tail current Itail. Almokalant and E-4031 prominently inhibited the rapidly activating inwardly rectifying component of the delayed K+ rectifier current in guinea pig ventricular myocytes, compared to d-sotalol and quinidine.

synapsesocial.com/papers/6a0e4e60bc348c84f2fd9ac8 https://doi.org/10.1093/cvr/26.11.1145

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Differential effects of the new class III antiarrhythmic agents almokalant, E-4031 and D-sotalol, and of quinidine, on delayed rectifier currents in guinea pig ventricular myocytes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Differential effects of the new class III antiarrhythmic agents almokalant, E-4031 and D-sotalol, and of quinidine, on delayed rectifier currents in guinea pig ventricular myocytes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

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