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Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
Published on: April 5, 2011
Cardiac arrhythmias induced by guanethidine in cats anesthetized with halothane
Insights
Guanethidine causes severe ventricular arrhythmias in cats under halothane anesthesia by releasing noradrenaline. This highlights the heart’s vulnerability to noradrenaline-releasing drugs during anesthesia.
Area of Science:
- Cardiology
- Pharmacology
- Anesthesiology
Background:
- Halogenated hydrocarbon anesthetics like halothane sensitize the heart to catecholamines.
- Guanethidine is known to affect adrenergic neurons.
Purpose of the Study:
- To investigate the arrhythmogenic potential of guanethidine in cats anesthetized with halothane.
- To compare the arrhythmias induced by guanethidine with those induced by noradrenaline.
- To elucidate the mechanism underlying guanethidine-induced arrhythmias.
Main Methods:
- Rapid intravenous administration of guanethidine and noradrenaline in halothane-anesthetized cats.
- Observation and characterization of induced ventricular arrhythmias.
- Assessment of the effects of beta-adrenoceptor blockers, imipramine, and reserpine on arrhythmias.
- Evaluation of arrhythmias after adrenergic neuron blockade.
Main Results:
- Guanethidine induced severe, sustained ventricular arrhythmias (e.g., ventricular tachycardia) lasting 4-100 minutes.
- Noradrenaline induced shorter-lasting ventricular arrhythmias (1-2.5 minutes).
- Beta-blockers prevented arrhythmias from both drugs; imipramine/reserpine blocked guanethidine-induced but not noradrenaline-induced arrhythmias.
- Guanethidine's arrhythmogenic effect persisted after adrenergic neuron blockade.
Conclusions:
- Guanethidine triggers cardiac arrhythmias by releasing noradrenaline from cardiac adrenergic neurons.
- The interaction between noradrenaline-releasing drugs and halogenated anesthetics increases cardiac vulnerability to arrhythmias.
Abstract:
Rapid i.v. administration of guanethidine provokes severe and sustained ventricular arrhythmias in cats anesthetized with halothane. The arrhythmias include premature ventricular excitations, multifocal ventricular rhythm, bigeminy, trigeminy and ventricular tachycardia. They begin in about 20 sec and last from 4 to 100 min. By comparison, a standard dose of noradrenaline (10 micrograms/kg) induces ventricular arrhythmias which develop in about 12 sec and continue for 1-2.5 min. Pretreatment with beta-adrenoceptor blocking drugs prevents arrhythmias from both drugs, and pretreatment with imipramine or reserpine prevents arrhythmias for guanethidine but not noradrenaline. The adrenergic neuron blocking action of guanethidine does not alter the arrhythmogenic action of guanethidine since arrhythmias can still be produced after adrenergic neuron blockade. These results indicate that guanethidine causes arrhythmias by releasing noradrenaline from cardiac adrenergic neuron storage sites and, therefore, point out the vulnerability of the heart to arrhythmias when noradrenaline-releasing drugs interact with halogenated hydrocarbon anesthetics.
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