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[Effects of N-ethyl perhexiline on His bundle electrogram in rabbits]
1Department of Pharmacology, School of Basic Medical Science, Beijing Medical University, China.
Zhongguo Yao Li Xue Bao = Acta Pharmacologica Sinica
|March 1, 1991
Summary
N-Ethyl perhexiline (NEP) prolongs cardiac conduction intervals in rabbits, indicating potential calcium-channel blockade. These findings suggest NEP may influence heart rhythm by affecting atrioventricular and intraventricular conduction.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
Background:
- N-Ethyl perhexiline (NEP) is a novel drug synthesized by the Department of Organic Chemistry, Beijing University.
- Understanding the cardiovascular effects of NEP is crucial for its potential therapeutic applications.
Purpose of the Study:
- To investigate the effects of N-Ethyl perhexiline (NEP) on atrioventricular (A-V) and intraventricular conduction in anesthetized rabbits.
- To elucidate the mechanism underlying NEP's cardiovascular effects, particularly its potential as a calcium-channel blocker.
Main Methods:
- Electrophysiological recordings in anesthetized rabbits, including His bundle electrogram (HBE) and electrocardiogram (ECG).
- Administration of varying doses of NEP (3 mg/kg and 6 mg/kg intravenously) to assess dose-dependent effects.
- Assessment of NEP's interaction with other agents like nicotinamide and isoproterenol to explore its mechanism of action.
Main Results:
- NEP administration significantly prolonged A-H, P-R, and R-R intervals in a dose-dependent manner.
- Higher doses of NEP (6 mg/kg) showed more pronounced prolongation of cardiac conduction intervals, including H-V interval.
- NEP demonstrated stronger effects on A-H and P-R intervals compared to perhexiline and antagonized the shortening effect of nicotinamide on the A-H interval.
Conclusions:
- The observed prolongation of A-H, P-R, and R-R intervals by NEP suggests a significant impact on cardiac conduction.
- NEP's ability to antagonize nicotinamide's effect and be inhibited by isoproterenol supports its role as a calcium-channel blocker.
- These findings indicate that NEP's cardiovascular effects are likely mediated through calcium-channel blockade, influencing cardiac electrophysiology.