What is the clinical evidence from this study?

Study design: Other. Population: Atrioventricular transmission. Intervention: Quinidine gluconate and potassium. Primary outcome: Atrio-ventricular (A-V) conduction time and action potential amplitude.

What does this research mean for the field?

Quinidine-induced prolongation of atrioventricular conduction time is antagonized by low extracellular potassium and enhanced by high potassium concentrations. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

April 1, 1967Circulation ResearchOpen Access

Interactions of Quinidine and Potassium on Atrioventricular Transmission

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Key result

High potassium enhances and low potassium antagonizes quinidine-induced AV conduction delay in rabbit hearts.

Population

Isolated, perfused rabbit hearts

Comparison

Quinidine gluconate added to normal vs low vs high potassium concentration

Design

Ex vivo microelectrode study

Authors

YWYoshio WatanabeShowa University LDLeonard S. DreifusAmerican College of Cardiology

Discussion

Member takes

Implication

Rabbit heart findings on quinidine-potassium AV effects are hypothesis-generating; leaves open human relevance.

Structured PICO

Population

Isolated, perfused rabbit hearts studied utilizing microelectrode techniques to assess atrioventricular conduction.

Intervention

Quinidine gluconate (10 mg/liter) added to perfusion fluid containing normal [K+] (4.5 mEq/liter), low [K+] (1.5 mEq/liter), or high [K+] (7.5 mEq/liter)

Outcome

Atrio-ventricular (A-V) conduction time and action potential amplitude in the A-V node regionssurrogate

In an isolated rabbit heart model, the prolongation of A-V conduction induced by quinidine is highly dependent on potassium concentrations, being antagonized by low potassium and enhanced by high potassium.

Cite This Study

Watanabe et al. (1967) studied Atrioventricular transmission. Quinidine gluconate and potassium was evaluated on Atrio-ventricular (A-V) conduction time and action potential amplitude. In isolated rabbit hearts, quinidine-induced prolongation of A-V conduction time was antagonized by low potassium and enhanced by high potassium concentrations.

synapsesocial.com/papers/6aa7e678eb815e3469da0f2f https://doi.org/10.1161/01.res.20.4.434

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April 1, 1967Circulation ResearchOpen Access

Interactions of Quinidine and Potassium on Atrioventricular Transmission

View Full Paper

Ask AI

Bookmark

Key result

High potassium enhances and low potassium antagonizes quinidine-induced AV conduction delay in rabbit hearts.

Population

Isolated, perfused rabbit hearts

Comparison

Quinidine gluconate added to normal vs low vs high potassium concentration

Design

Ex vivo microelectrode study

Authors

YWYoshio WatanabeShowa University LDLeonard S. DreifusAmerican College of Cardiology

Discussion

Member takes

Implication

Rabbit heart findings on quinidine-potassium AV effects are hypothesis-generating; leaves open human relevance.

Structured PICO

Population

Isolated, perfused rabbit hearts studied utilizing microelectrode techniques to assess atrioventricular conduction.

Intervention

Quinidine gluconate (10 mg/liter) added to perfusion fluid containing normal [K+] (4.5 mEq/liter), low [K+] (1.5 mEq/liter), or high [K+] (7.5 mEq/liter)

Outcome

Atrio-ventricular (A-V) conduction time and action potential amplitude in the A-V node regionssurrogate

Cite This Study

synapsesocial.com/papers/6aa7e678eb815e3469da0f2f https://doi.org/10.1161/01.res.20.4.434

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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