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Biomedical subjects

H Refsum

Publications and source records attributed to H Refsum.

At least 253 records · Page 14Linked to original sources
PubMed1975

Effects of N-acetylprocainamide as compared with procainamide in isolated rat atria.

The actions of procainamide and its major metabolite N-acetylprocainamide were tested and compared on isolated rat atria. While procainamide exerted a negative chronotropic and iontropic effect, N-acetylprocainamide had the opposite effect. It is suggested that a N-acetylprocainamide-induced increase in myocardial work can counteract the negative inotropic action of procainamide and thus to some extent explain the variable results with the latter compound on myocardial performance reported from in vivo experiments. Procainamide increased the refractory period and reduced the excitability of isolated rat atria. N-acetylprocainamide, on the other hand, caused negligible effects on these parameters.

Animals↗
PubMedDate not supplied

Arrhythmogenic and cardiodepressive effects of contrast media on isolated rat atria.

The cardiotoxicity of four radiopaque contrast media were studied on spontaneously beating isolated rat atria in order to compare the low-osmolar non-ionic medium, metrizamide, with three other contrast media having different cation compositions. The addition of the ionic contrast media to concentrations of 28 and 84 mg I/ml induced atrial arrhythmias in the following order of potency: meglumine iothalamate greater than meglumine--Na--Ca metrizoate greater than meglumine--Na diatrizoate. No arrhythmias were observed after the addition of metrizamide. Metrizamide had only slight effects on the rate and amplitude of the atrial contractions, and hence the work index was almost unaffected. The highest concentration of the three ionic contrast media had very significant cardiodepressive effects. Meglumine iothalamate had the most severe influence on the spontaneous rate of the contractions, while meglumine--Na diatrizoate induced the greatest initial reduction in the amplitude of the contractions and the work index. The present study indicates that the low-osmolar non-ionic medium, metrizamide, is better tolerated by the myocardium than the ionic contrast media.

Animals↗
PubMedDate not supplied

Vagus-induced changes in ventricular electrophysiology of the dog heart with and without beta-blockade.

We tested the electrophysiologic effects of vagus stimulation in six dogs in the presence or absence of beta-adrenoreceptor blockade. Monophasic action potentials were obtained by the suction electrode technique and programmed electrical stimulation was used to determine heart rate-independent changes in 50 and 90% repolarization times and in the effective (V-ERP) and functional (V-FRP) refractory periods of the right ventricle. Vagus stimulation decreased heart rate both in the presence and in the absence of beta-adrenoceptor blockade. It also increased action potential duration and refractoriness during high sympathetic tone induced by pentobarbital anesthesia. The effect is probably due mainly to inhibition of beta 1-adrenoreceptors, since it was decreased by beta 1-adrenoceptor blockade with atenolol. We conclude that stimulation of the vagus has antiarrhythmic effects in ventricles under high sympathetic stimulation.

Acetylcholine↗
PubMedDate not supplied

Prolonged ventricular refractoriness and action potential duration after beta-adrenoreceptor blockade in the dog heart in situ.

We studied the effects of three different beta-adrenoreceptor-blocking drugs (atenolol, acebutolol, and propranolol) on the duration of monophasic action potentials and refractoriness of the right ventricular myocardium in closed-chest dogs. Pentobarbital anesthesia, which is known to increase the sympathetic tone, was used. Monophasic action potential recordings were obtained by the suction electrode technique, and refractoriness was measured by means of programmed electrical stimulation. A stepwise decrease in stimulation intervals from 350 to 300, 260, and 230 ms caused a progressive decrease in refractoriness as well as in the duration of the monophasic action potential. Intravenous injections of atenolol 0.5 mg/kg, acebutolol 2.0 mg/kg, and propranolol 0.5 mg/kg after pretreatment with atropine each increased the times for 50 and 90% repolarization of the monophasic action potential at each stimulation interval. The effective and the functional refractory periods paralleled the changes in the action potential duration in all experiments. We conclude that beta-adrenoreceptor blockade in the presence of adrenergic receptor stimulation prolongs ventricular refractoriness and action potential duration, and that the presence or absence of cardiac selectivity or slight intrinsic sympathomimetic activity plays no role in this process. These results suggest that if the antiarrhythmic action of beta-blocking drugs is due to prolongation of ventricular refractoriness, all types of these drugs may be expected to be equally effective as therapeutic agents.

Action Potentials↗
PubMedDate not supplied

Vasodilator and inotropic effects of the antiarrhythmic drug melperone.

We investigated the hemodynamic and inotropic effects of the new class III antiarrhythmic drug melperone. In eight pentobarbital-anesthetized dogs, the effects of intravenous melperone 0.5, 2.5, and 12.5 mg/kg-1 were tested. During atrial pacing we measured cardiac output (CO), mean aortic blood pressure (MAP), right (RV) and left (LV) ventricular pressures, and LV dP/dt. In six RV papillary muscles isolated from cats and suspended in a muscle bath containing Krebs-Henseleit solution, we studied the direct effects of melperone 10(8)-5 X 10(-5) M. Administration of melperone decreased total peripheral resistance, MAP, RV and LV systolic and end-diastolic pressures, while CO remained unchanged. Melperone increased LV dP/dtmax. The contractile force (F) and dF/dtmax of the isolated ventricular muscle preparations increased slightly with increasing concentrations of melperone, up to 10(-5) M. In conclusion, melperone has vasodilator and slight positive inotropic effects in addition to its class III antiarrhythmic effect.

Animals↗
PubMedDate not supplied

Class III antiarrhythmic action in experimental atrial fibrillation and flutter in dogs.

Progress in the pharmacological treatment of atrial fibrillation and flutter has been achieved by the introduction of the class III antiarrhythmic drug amiodarone. In the present study we tested amiodarone and a new class III antiarrhythmic drug, melperone, in experimentally induced atrial fibrillation and flutter in pentobarbital-anesthetized dogs. By high-rate stimulation in the right atrium, atrial fibrillation was induced in 4, and atrial flutter in 10 out of 22 dogs. Atrial flutter rate was 496 +/- 13 min-1 (median +/- 95% confidence interval). Both drugs converted the arrhythmias at doses from 2.5 to 10 mg . kg-1 and reduced that atrial flutter rate before conversion. Average ventricular rate during arrhythmias (261 +/- 16 min-1) decreased after amiodarone, and was unchanged or, in three out of nine dogs, increased after melperone. The doses of amiodarone converting the arrhythmias increased atrial refractoriness, whereas the effects on AV nodal conduction and refractoriness were variable. The results support the concept that atrial flutter is due to circus movement where the flutter rate is dependent upon atrial refractoriness. The class III antiarrhythmic drugs amiodarone and melperone seem to be equally potent in converting atrial arrhythmias.

Amiodarone↗
PubMedDate not supplied

Changes in ventricular fibrillation threshold during acute hypothermia. A model for future studies.

Hypothermia and rewarming are associated with an increased incidence of lethal arrhythmias in man. The relationship between reduction in body temperature and ventricular fibrillation threshold was studied in 7 pentobarbital anaesthetized dogs using programmable electrical stimulation while cooling and rewarming between 37 degrees C and 25 degrees C in steps of 3 degrees C. Fibrillation threshold was defined as the number of extrastimuli required to evoke ventricular fibrillation. QRS-durations and corrected QT-intervals (QTc) were measured from surface electrocardiograms. Monophasic action potential durations were recorded from the base and apex of the heart. Fibrillation threshold decreased with decreasing temperatures; e.g., at 37 degrees C ventricular fibrillation was not inducible after 5 extrastimuli, while at 25 degrees C only 2 extrastimuli were required. From 37 degrees C to 25 degrees C QRS-width, monophasic action potential durations and QTc increased while conduction velocity decreased. The differential effects on conduction and monophasic action potential duration provide a basis for induction of ventricular fibrillation during acute hypothermia. This model of hypothermia-induced ventricular fibrillation should prove useful for future studies aimed at understanding the mechanisms responsible for hypothermia-related deaths.

Action Potentials↗