What is the clinical evidence from this study?

Study design: Other. Population: Ischemic isolated rabbit hearts. Intervention: Procainamide and N-Acetylprocainamide. Primary outcome: Myocardial contractility (dP/dt).

What does this research mean for the field?

N-acetylprocainamide depresses myocardial contractility at high infusion rates (≥40 mg/min) and lacks direct intrinsic positive inotropic activity in isolated ischemic myocardium. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

December 1, 1981Experimental Biology and Medicine

Effects of Procainamide and N-Acetylprocainamide on Myocardial Contractility in Ischemic Isolated Rabbit Hearts

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Key result

N-acetylprocainamide depresses dP/dt at 40 mg/min and lacks positive inotropic activity in ischemic rabbit hearts.

Why the study?

Does N-acetylprocainamide have intrinsic direct positive inotropic activity compared to procainamide in ischemic isolated rabbit hearts?

Population

Isolated, perfused, globally ischemic rabbit hearts (including a subset pretreated with reserpine)

Comparison

N-acetylprocainamide vs Procainamide

Design

Preclinical

Authors

JKJeffrey KlugerElectrophysiology HHHeidi C. HornerAthena Group (United States)MRM M ReidenbergCornell University

Discussion

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Implication

Lacks direct inotropic activity in ischemic rabbit hearts; leaves open catecholamine-mediated effects for in vivo study.

Structured PICO

Does N-acetylprocainamide have intrinsic direct positive inotropic activity compared to procainamide in ischemic isolated rabbit hearts?

Population

Isolated, perfused, globally ischemic rabbit hearts (including a subset pretreated with reserpine)

Intervention

N-acetylprocainamide (infusion rates ranging from ~1 mg/min to 40 mg/min or greater)

Comparator

Procainamide (infusion rates of 2 mg/min or greater)

Outcome

Myocardial contractility measured by dP/dtsurrogate

N-acetylprocainamide does not possess intrinsic direct positive inotropic activity in the isolated ischemic rabbit heart model, and its apparent inotropic effects at low doses are likely catecholamine-mediated.

Cite This Study

Kluger et al. (1981) studied Ischemic isolated rabbit hearts. Procainamide and N-Acetylprocainamide was evaluated on Myocardial contractility (dP/dt). N-acetylprocainamide depressed dP/dt at infusion rates ≥40 mg/min and lacks intrinsic direct positive inotropic activity in isolated ischemic rabbit hearts.

synapsesocial.com/papers/6aa882aebdf837821459b34e https://doi.org/10.3181/00379727-168-41285

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Effects of Procainamide and N-Acetylprocainamide on Myocardial Contractility in Ischemic Isolated Rabbit Hearts

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Effects of Procainamide and N-Acetylprocainamide on Myocardial Contractility in Ischemic Isolated Rabbit Hearts

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

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