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Biomedical subjects

J Toyama

Publications and source records attributed to J Toyama.

At least 19 recordsLinked to original sources
PubMed1979

Effect of cardiotonic polypeptide anthopleurin-A on canine Purkinje and ventricular muscle fibers.

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.

Action Potentials↗
PubMed1979

Body surface potential distributions in posterior ventricular pre-excitation.

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.

Action Potentials↗
PubMed1979

Effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker in awake dogs.

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.

Animals↗
PubMed1979

Inhomogeneous spread of excitation in canine Purkinje fibers.

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.

Animals↗
PubMed1979

[Renal failure].

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Humans↗
PubMed1979

Antiarrhythmic effects of L-penbutolol and DL-propranolol. Comparison of the effects of these two drugs on conductivity and excitability in canine heart in vivo.

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.

Animals↗
PubMed1978

Computational reconstruction of body surfact isopotential maps in myocardial infarction: comparison between nontransmural and transmural infarction.

The relationship between the lack of electromotive force in myocardial infarction and body surface potential distribution was investigated on maps reconstructed from a simulated heart model and transfer impedance vectors of human torso model. The heart model, a cluster of 3-mm cubic blocks, was stored in the memory of a computer. Transfer impedance vectors between 81 lead points on the human torso model and 392 positions covering ventricular areas in the torso were measure. Body surface potential values were calculated mathematically by summing up scalar products between the electromotive force of the heart model and the measured transfer impedance vectors. Thus, reconstructed maps changed in their patterns with the alternation in lacation and/or extent of infarcted region in the heart model. In particular, the appearance of the abnormal potential minimum, which projects the infarcted region in the heart model onto the torso surface, was characteristic in both transmural and subendocardial infarction. In addition, delayed activation in the intact layer of the epicardium overlying the infarcted region produced a potential maximum on the same place as the abnormal potential minimum appeared previously.

Action Potentials↗
PubMed1978

Body surface isopotential maps. Clinical application to the diagnosis of myocardial infarction.

This paper is a review of recent work relating body surface isopotential maps to the detection of the site and extent of myocardial infarction in cases which are either indetectable or difficult to diagnose through the use of standard 12 lead ECGs. According to the difference of the site and extent of myocardial infarction, the characteristic maps are obtained. Through the use of body surface isopotential maps, the significant clinical information may be obtained in a number of cases, and we can do better with mapping than without it in the evaluation of patients with myocardial infarction.

Adult↗