ABSTRACT
1. The effects of acetylcholine (ACh) on cardiac rate (electrocardiogram), contractile force and coronary flow recorded simultaneously were investigated in isolated guinea pig hearts perfused with Locke solution by the method of Langendorff. 2. Bolus injections of 0.5-550 nmol ACh induced oscillations of cardiac rate. These changes were not directly related to the doses of ACh injected (chi 2 test, P greater than 0.05). 3. The presence of 10 microM physostigmine in the Locke solution increased the number of heart rate oscillations elicited by ACh. 4. The electrocardiogram showed that the heart rate oscillations were due to wandering pacemakers, such as slow or fast junctional rhythm, and slow or fast idioventricular rhythm, which were intermingled with sinus rhythm, A-V block or sinus bradycardia. 5. In most experiments, the increase in ventricular rate was associated with an increase in ventricular contractile force ("Bowditch Effect") and a simultaneous reduction of coronary flow. 6. The heart rate oscillations were not prevented by reserpine or blockade of nicotinic receptors (hexamethonium plus gallamine) but were prevented by blockade of muscarinic receptors with atropine. 7. We conclude that the heart rate oscillations induced by ACh are due to several electrophysiological mechanisms (automatism and/or conduction disturbances) related to activation of muscarinic receptors.
Subject(s)
Acetylcholine/administration & dosage , Coronary Circulation/drug effects , Heart Rate/drug effects , Myocardial Contraction/drug effects , Animals , Arrhythmias, Cardiac/chemically induced , Electrocardiography , Guinea Pigs , Male , Perfusion , Reserpine/administration & dosageABSTRACT
1. The effects of acetylcholine (ACh) on cardiac rate (electrocardiogram), contractile force and coronary flow recorded simultaneously were investigated in isolated guinea pig hearts perfused with Locke solution by the method of Langendorff. 2. Bolus injections of 0.5-550 nmol ACh induced oscillations of cardiac rate. These changes were not directly related to the doses of ACh injected (X**2 test, P > 0.05). 3. The presence of 10 micronM physostigmine in the Locke solution increased the number of heart rate oscillations elicited by ACh. 4. The electrocardiogram showed that the heart rate oscillations were due to wandering pacemakers, such as slow or fast junctional rhythm, and slow or fast indioventricular rhythmy, which were intermingled with sinus rhythym, A - V block or sinus bradycardia. 5. In most experiments, the increase in ventricular rate was associated with an increase in ventricular contractile force ("Bowditch Effect") and a simultaneous reduction of coronary flow. 6. The heart rate oscillations were not prevented bu reserpine or blockade of nicotinic receptors (hexamethonium plus gallamine) but were prevented blockade of muscarinic receptors with atropine. 7. We conclude that the heart rate oscillations induced by ACh are due to several electrophysiological mechanisms (automatism and/or conduction disturbances_ related to activation of muscarinic receptors
Subject(s)
Guinea Pigs , Animals , Male , Acetylcholine/pharmacology , Myocardial Contraction , Heart Rate , Blood Flow Velocity , ElectrocardiographyABSTRACT
To study the cardiac effects induced by purified scorpion toxin (tityustoxin, TsTX), without circulatory and respiratory influences, isolated guinea pig hearts were used. Single injections of 10, 20 or 30 micrograms TsTX induced positive inotropic and chronotropic effects in the majority of the experiments. The inotropic effects were dose-dependent. Simultaneous recording of the electrical activity of the heart showed sinus tachycardia, T wave inversion and ST segment deviations. Sinus bradycardia and/or A-V block were recorded in some experiments, simultaneously with the positive inotropic effects. After these initial events, the larger dose of TsTX elicited periodic changes of heart rate (in 70% of the experiments) which were explained by wandering pacemakers. During these periodic changes in heart rate, the electrocardiogram showed sinus bradycardia, idioventricular rhythm, complete or partial A-V block, sinus tachycardia, sinus arrest and junctional rhythm. The coronary flow varied inversely with the inotropism and the cardiac rate, but the changes in flow were related mainly to the inotropism. The effects of TsTX on the electrocardiogram, inotropism and coronary flow spontaneously disappeared 15-20 min after toxin injection. The arrhythmias induced by TsTX were blocked either by propranolol or by atropine and are assumed to be due to the release of catecholamines and acetylcholine from postganglionic nerve fibers in the heart.
