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Cocaethylene causes dose-dependent reductions in cardiac function in anesthetized dogs
L D Wilson1, R J Henning, C Suttheimer
1Department of Emergency Medicine, Mt. Sinai Medical Center Cleveland, Ohio 44106, USA.
Journal of Cardiovascular Pharmacology
|December 1, 1995
Summary
Cocaethylene, a metabolite from combining cocaine and ethanol, significantly depresses heart function. This study in dogs shows cocaethylene impairs cardiac contractility, reduces blood pressure, and alters heart rhythms, contributing to cardiotoxicity.
Area of Science:
- Cardiovascular Pharmacology
- Toxicology
Background:
- Cocaine and ethanol co-abuse is common, leading to severe toxicity.
- Cocaethylene, a unique metabolite formed from this combination, is implicated in adverse effects.
- Understanding cocaethylene's cardiovascular impact is crucial for managing toxicity.
Purpose of the Study:
- To investigate the direct cardiovascular effects of cocaethylene.
- To quantify the impact of cocaethylene on cardiac function and electrophysiology.
Main Methods:
- Intravenous administration of varying doses of cocaethylene to mongrel dogs.
- Continuous monitoring of electrocardiogram (ECG) and hemodynamic parameters (pressures, cardiac output).
- Assessment of ventricular contractility and relaxation using dP/dtmax and dP/dtmin.
Main Results:
- Cocaethylene significantly decreased left ventricular contractility (dP/dtmax) and relaxation (dP/dtmin).
- Reduced stroke volume and mean arterial pressure were observed at higher doses.
- Prolonged QRS and QTc intervals indicated significant ECG abnormalities.
- Hemodynamic and ECG changes persisted for extended periods.
Conclusions:
- Cocaethylene exhibits potent myocardial depressant effects.
- It significantly alters cardiac contractility, hemodynamics, and cardiac electrical activity.
- Cocaethylene is a likely major contributor to the cardiotoxicity observed in combined cocaine and ethanol users.