PT  - JOURNAL ARTICLE
AU  - S W Rabkin
AU  - J M Friesen
AU  - J A Ferris
AU  - H Y Fung
TI  - A model of cardiac arrhythmias and sudden death: cantharidin-induced toxic cardiomyopathy.
DP  - 1979 Jul 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 43--50
VI  - 210
IP  - 1
4099  - http://jpet.aspetjournals.org/content/210/1/43.short
4100  - http://jpet.aspetjournals.org/content/210/1/43.full
SO  - J Pharmacol Exp Ther1979 Jul 01; 210
AB  - Toxic cardiomyopathy may result in fatal arrhythmias. To develop a model to study ventricular fibrillation and asystole, we investigated the effect of cantharidin in the production of cardiac arrhythmias and myocardial damage. Conscious albino rabbits, weighing between 1.8 to 2.8 kg received an intravenous bolus injection of cantharidin ranging from 0.6 to 1.9 mg/kg or a control injection of solvent. The electrocardiogram was continuously monitored on tape before and after injection for extended periods of time. Dose-related effects were observed with the following: 1) presence, magnitude and duration of ST depression after injection; 2) occurrence of fatal arrhythmias; 3) survival time (high doses were usually fatal within 3 hr); and 4) electron microscopic evidence of mitochondrial swelling, intramitochondrial granules and myofibrillar degeneration. The most common arrhythmias associated with the high doses of cantharidin were frequent ventricular ectopics, ventricular tachycardia, ventricular fibrillation or asytole. The arrhythmias could not be explained by alterations in blood pressure, electrolytes or blood gases. These findings show the cardiotoxic properties of cantharidin and its ability to produce fatal cardiac arrhythmias. Thus, it may serve as a model to study sudden death and the efficacy of antiarrhythmic drugs.