Post-overdrive suppression of the rabbit sinus node pacemaker cells.
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Biomedical subjects
Publications and source records attributed to J Toyama.
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Effects of Anthopleurin-A (AP-A, polypeptide from sea anemone) were studied on electrophysiological properties of isolated canine Purkinje and ventricular muscle fibers. Ap-A (in concentrations above 20 micrograms/l) produced a dose-dependent increase in action potential duration (APD) and the refractory period (RFP) in electrically driven Purkinje fibers, but had no effect on other parameters. Similar but less prominent change in APD and RFP was observed in ventricular muscle fibers. AP-A in high concentrations (200 micrograms/l or higher) did alter the spontaneous firing rate of Purkinje fibers. Since AP-A in low concentrations will increase the refractory period of conducting fibers without affecting a conduction velocity, it may abolish some re-entrant arrhythmias.
Waveform of the QRS complex during ventricular pre-excitation is subject to the influence of both the site of pre-excitation and the time of pre-excitation relative to that of excitation via the normal AV path. This paper reports a case in which lead V1 of the electrocardiogram (ECG) could be altered from an R to an rS pattern by the administration of atropine sulfate. The provable mechanism was that of reduced conduction time in the normal AV path with altered time phase of normal excitation and pre-excitation. This mechanism was simulated in experiments on dogs and yielded similar findings. Body surface mapping in both the patient and the dogs provided evidence that pre-excitation could be recognized by that means with varied time phase of normal excitation and pre-excitation. It was demonstrated that the QRS complex of right sided precordial leads could be altered from an R to an rS pattern by altering the time phase of normal excitation and pre-excitation of the posterior ventricular wall. This alteration was related to the degree to which negative potentials on the anterior chest wall due to right ventricular breakthrough of normal activation developed in relation to the time of pre-excitation.
The effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker was evaluated in 15 awake dogs with experimentally induced A-V junctional rhythm. The duration of asystole after overdrive (D.A.O.) in these dogs was prolonged significantly in accordance with increase in the drive rate, and the mean +/- SD of the D.A.O. reached 4.7 +/- 1.1 seconds (N = 15) after overdrive at 2.5 times the spontaneous heart rate. After administration of atropine (0.4 mg/kg; i.v.) to eight dogs, the mean +/- SD of the D.A.O. at the same rate decreased from 4.5 +/- 0.9 to 3.4 +/- 1.2 seconds. After administration of practolol (0.5 mg/kg; i.v.) to the seven other dogs, the mean +/- SD of the D.A.O. at the same rate increased remarkably from 4.9 +/- 1.3 to 9.4 +/- 3.0 seconds. Intravenous injection of practolol (0.5 mg/kg) had no effect upon the D.A.O. in the five dogs with sinus rhythm. Thus, it is suggested that (1) the sympathetic nerve might play a more important role in regulating the automaticity of the A-V junctional pacemaker than the vagus and (2) it physiologically might take over 5.0 seconds for the A-V junctional pacemaker to initiate an escape beat during longstanding sinus arrest, if a marked dysfunction of the A-V junctional pacemaker occurs due to a decrease in tension of the sympathetic nerve.
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Spread of excitation in isolated canine bundle branches was examined by microelectrode technique in order to investigate the possibility of dissociated impulse transmission in normal Purkinje fibers. In all experiments, local excitation of the preparation evoked either by fine bipolar extracellular electrodes or an intracellular microelectrode proceeded much faster along the longitudinal axis of the fibers than along the transverse axis. As a result, the spread of excitation in the vicinity of stimulating site showed significantly inhomogeneous character. The inhomogeneity of excitation spread became more manifest with more eccentric location of the stimulating site in a given preparation. Larger preparation showed greater degree of inhomogeneity. Nevertheless, the inhomogeneous spread of excitation alone appeared unlikely to provide multiply pathways which were functionally dissociated with each other. When premature stimulation was applied, however, different conductivity among fibers within a single false tendon was oberved, suggesting that each conducting element became more independent.
The effects of l-penbutolol and dl-propranolol on A-V conduction, on excitability of ventricular muscle, and on ventricular tachycardia threshold in acute ischemia were compared, using anesthetized dogs. 1. L-penbutolol (100 microgram/Kg) and dl-propranolol (100 microgram/Kg) prolonged A-V conduction and reduced excitability of ventricular muscle significantly. L-penbutolol less prolonged A-V conduction than dl-propranolol. 2. Both l-penbutolol (50 microgram/Kg) and dl-propranolol (50 microgram/Kg) significantly prevented the lowering of ventricular tachycardia threshold in acute ischemia. These beta-blocking drugs are effective in the treatment of arrhythmia and l-penbutolol could be used safely, because of its weaker inhibition on A-V conduction.
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