ISSN:
1432-1912
Keywords:
Antifibrillatory Agents
;
Aconitine
;
Cardiac Output
;
Blood Pressure
;
Therapeutic Index
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary 1. Antiarrhythmic activity in anesthetized rats was assessed for eight antiarrhythmic drugs by determining the dose which increases the arrhythmic dose of aconitine by 50% (i.e. from 25.4 up to 38.1 μg/kg). According to their anti-aconitine ED50 the antiarrhythmics revealed the following decreasing order of potency: ajmaline 〉 propranolol 〉 sparteine 〉 brufacaine 〉 quinidine 〉 lidocaine 〉 phenytoin 〉 procainamide. 2. In a second series of experiments we infused intravenously in rats the anti-arrhythmic drugs (a tenth of the anti-aconitine ED50 per min) and determined cardiac output, heart rate, stroke volume, arterial blood pressure, and peripheral resistance. The infusion of the anti-aconitine ED50 of lidocaine, propranolol, sparteine, and brufacaine reduced cardiac output by 38, 36,18, and 17.5%, respectively. This decrease of cardiac output was caused by a strong bradycardia not compensated by an enhanced stroke volume. 3. Cardiac output was not significantly decreased by ajmaline, procainamide, quinidine, and phenytoin. Peripheral resistance was reduced after ajmaline and quinidine. The strong cardiodepressive action of lidocaine in rats is, to an essential extent, caused by the drug's inhibitory influence on respiration since, in artificially ventilated animals, cardiac output was reduced by 14% only. 4. In anesthetized cats all antiarrhythmics, except brufacaine, reduced cardiac output via bradycardia not compensated by increased stroke volume. 5. Experiments using harmine which has mainly negative chronotropic activity confirmed the view that bradycardia without increased stroke volume is indicative of negative inotropic action.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00997124
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