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Biomedical subjects

J Toyama

Publications and source records attributed to J Toyama.

At least 163 records · Page 9Linked to original sources
PubMed1984

Body surface isopotential maps of normal Japanese children.

Body surface isopotential maps were compared between 52 normal children and 47 normal adults. While sequential changes in body surface potential distribution were similar, 4 significant differences in body surface maps were observed between them: 1) Surface maps of normal children showed less smooth contour of isopotential lines than did those of normal adults. For example, breakthrough minimum was recognized more frequently in children (100%) than adults (65%). 2) Breakthrough minimum appeared earlier in normal children (23.2 +/- 5.0 msec) than in normal adults (29.2 +/- 4.3 msec), and more leftwards on the chest. 3) Forty-seven percent of the children showed positive potentials on the upper and right portions of the anterior chest in the terminal phase of QRS, but this pattern was not observed in normal adults. 4) The maximum at the time of the peak of the T wave appeared more leftward in normal children than normal adults.

Adolescent↗
PubMed1983

Comparative evaluation of depressed automaticity in sick sinus syndrome by Holter monitoring and overdrive suppression test.

To ascertain whether the long cardiac pauses on the Holter ECGs of patients with the sick sinus syndrome were related to the spontaneously occurring overdrive suppression, the heart rates for the 12 seconds preceding the cardiac pauses longer than 5 seconds were compared with that averaged for 24 hours. Even in six out of seven patients with bradycardia-tachycardia syndrome the former rate was not significantly greater than the latter, indicating that episodes of such long cardiac pauses may not result from spontaneously occurring overdrive suppression. This observation was also consistent with the result that no statistically significant correlation was obtained between the maximum pauses measured from Holter ECGs of sick sinus syndrome and those obtained by the overdrive suppression test. In conclusion, many episodes of long life-threatening cardiac pauses observed in sick sinus syndrome may be attributed to accidental depression of the sinus nodal and subsidiary pacemaker activity rather than to spontaneously occurring overdrive suppression; therefore, Holter monitoring may be useful as an additional tool for diagnosis of sick sinus syndrome.

Adolescent↗
PubMed1983

Experimental studies on sick sinus syndrome: relationship of extent of right atrial lesions to subsidiary pacemaker shift and its function.

An area where the sinus node was located in 36 dogs was defined as the "SN-area." Five to 7 days after cauterization of the SN-area, a subsidiary pacemaker remained in the SN-area in seven (group S) and shifted to outside the SN-area in 14 dogs (group E). The SN-area in group S had escaped complete destruction, but that in group E was destroyed completely. Heart rate in group S and group E was 154.0 +/- 27.1 and 107.6 +/- 16.8 beats/min (p less than 0.001), respectively. Maximum duration of asystole after overdrive (maxDAO) in group S and group E was 656.7 +/- 260.2 and 2470.2 +/- 2271.6 msec (p less than 0.01), respectively. Propranolol (0.2 mg/kg intravenously) decreased heart rate in group S and group E to 88.3 +/- 7.9 and 71.7 +/- 8.7% (p less than 0.001), and prolonged maxDAO to 140.1 +/- 28.1 and 492.7 +/- 591.4% (p less than 0.025), respectively. It is concluded that the rate and stability of subsidiary pacemakers after cauterization of the sinus node have a close relationship with their location in the right atrium, which is dependent on the extent of lesions in the SN-area. Sympathetic tone played a significant role in maintaining these functions in group E.

Animals↗
PubMed1983

Effects of timing of vagal stimulation on the sinoatrial nodal cell discharge.

The effects of vagal stimulation on the activity of the isolated rabbit sino-atrial (SA) node preparation were studied using electrophysiological techniques. Brief stimulus trains, which were subthreshold for the myocardial cells, were applied in order to release acetylcholine (ACh) from the nerve terminals. Transmembrane potentials were recorded from the follower cells located at the exit site near the pacemaker region. As the time from peak of the action potential to delivery of the vagal stimuli was progressively increased, the sinus cycle length first became progressively prolonged, and then was rapidly reduced to the control value. In order to resolve the underlying mechanisms for the phase-dependency, the effects of vagal stimulation were examined in a quiescent SA node preparation. When one stimulus was applied, membrane hyperpolarization began after a latency of 70 msec and developed slowly, reaching its peak value after about 270 msec, and its total time course was about 630 msec. Oscillatory potentials were observed after the recovery of the vagal-induced hyperpolarization; such oscillations were not observed in atrial myocardial cells. It is concluded that the slow-onset long-lasting response of the SA node cell membrane to ACh may play a role in the phase-dependent effect of vagal stimulation.

Acetylcholine↗
PubMed1983

Epicardial activation patterns and dispersion of refractoriness initiating ventricular tachycardia in the canine left ventricle during acute ischemia.

We examined the activation patterns in the left ventricular epicardial surface of dog hearts using multielectrode grid during the beats initiating ventricular tachycardia 5 to 120 min after coronary artery occlusion. The grid was placed on the ischemic border zone (the area was confirmed by ST-isopotential mapping) to record simultaneously 36 unipolar epicardial potentials. Under the control conditions almost radial spread of activation from the central stimulating electrode of the grid was observed. Activation during acute ischemia showed crowded isochrone lines in the ischemic area, especially during the premature beats with shorter coupling intervals. In 8 out of 15 episodes, where ventricular tachycardia was induced by a single premature stimulus, the conduction delay during premature beats culminated in the local conduction block accompanied by circus movement of activation. Subsequent initial beats of ventricular tachycardia also showed similar activation patterns indicating reentry of excitation. In the remaining 7 episodes, however, we could not obtain such circus movement of activation under the grid. We also measured the effective refractory period at 5 sites under the grid. The results showed greater dispersion of the effective refractory period in the ischemic border zone throughout 5 to 120 min after coronary occlusion in the cases where ventricular tachycardia developed. These findings suggest that reentry of excitation, which is most probably caused by inhomogeneity of refractoriness in the ischemic border zone, may play an important role in the genesis of ventricular tachyarrhythmias during acute ischemia.

Animals↗
PubMed1983

The electrophysiological actions of lidocaine on ischemic ventricular muscle as compared with procainamide.

For the purpose to evaluate the effects of lidocaine on the ventricular arrhythmias occurring as complications of acute myocardial ischemia or infarction, the electrophysiological actions of lidocaine were estimated, as compared with those of procainamide, on the right ventricular papillary muscle of the rabbit heart superfused with hypoxic, hyperkalemic and/or acidic Krebs-Ringer solution. Lidocaine (1 to 5 x 10(-5)M) and procainamide (1.7 to 3.4 x 10(-5)M) depressed the maximum rate of action potential upstroke (Vmax) and prolonged both of the effective refractory period (ERP) and the diastolic interval needed for the premature Vmax to recover to 98% in magnitude of the basic Vmax (98% recovery time) dose-dependently, without decreasing the resting potential. Among the ischemic components, low pH (pH 6.9) and high potassium (10 mM) extracellular environments potentiated the depressant actions of lidocaine in synergic manner, but no significant enhancement of the actions of procainamide were observed under exposure to any components of ischemia. Mechanisms underlying the difference of the depressant actions on ischemic myocardium between lidocaine and procainamide were discussed in the light of recent concepts of actions of local anesthetics, and came to the conclusion that lidocaine is the most preferable antiarrhythmic agent for the management of ventricular arrhythmias during acute ischemia or infarction.

Action Potentials↗
PubMed1983

Sequential changes in the difference maps of potential distributions and the extent of myocardial infarctions.

Surface isopotential maps were recorded immediately before and 1 week after production of myocardial infarctions in 15 dogs. Difference maps were made by subtracting pre-infarction maps from time-equivalent post-infarction maps, and the electrophysiological basis of the difference maps was examined. The dogs were classified into 4 groups according to the location and extent of the infarction. Difference maps of these groups displayed an area with significant surface potential defects due to infarction. These changes were observed during specific phases of ventricular activation and in specific portions of the chest surface, depending on the location and extent of the infarction. These findings were well accounted for by the hypothesis that difference maps reflect the loss of activation fronts as a result of the infarction.

Animals↗
PubMed1983

Effects of hypoxia on conduction velocity of ventricular muscle.

The effects of hypoxia on the conduction of excitation in ventricular muscle were examined. Transmembrane action potentials and isometric tension of isolated rabbit papillary muscle were monitored simultaneously. When the preparations were exposed to hypoxia, the action potential duration (APD) shortened progressively and conduction velocity, assessed by the interval between two action potentials, decreased appreciably. This conduction delay was always accompanied by an increase in resting tension (RT). The upstroke velocity of the action potentials, however, was virtually unaffected by 60 min of hypoxia. When the perfusate was reoxygenated, the APD, conduction velocity and RT recovered. The conduction delay and elevation of RT due to hypoxia were prevented by verapamil or a low [Ca]0 medium and were potentiated by isoproterenol. These results suggest that a cytoplasmic Ca++ accumulation, resulting in intercellular electrical uncoupling, may contribute to the conduction delay during hypoxia.

Action Potentials↗
PubMed1983

Reflex control of ventricular refractoriness in the nonischemic myocardium during coronary occlusion.

The purpose of the study was to determine whether activation of cardiac receptors and arterial baroreceptors by myocardial ischemia could elicit reflex alteration of the effective refractory period (ERP) of nonischemic ventricular myocardium in cats. Changes in ERP of nonischemic area of the right ventricle and mean arterial pressure (MAP) were measured during transient left anterior descending (LAD) coronary artery occlusion in anesthetized cats. LAD coronary occlusion for 90 sec caused a small but significant shortening of ERP (maximal change = 2.5 +/- 2.3 msec) associated with a decrease in MAP. Vagotomy significantly augmented the shortening of ERP to -3.4 +/- 1.6 msec and attenuated the decrease in MAP. After selective cardiac sympathectomy, the reflex response in refractoriness was virtually abolished. In cats with sinoaortic denervation with intact sympathetic nerves, marked attenuation was observed in the reflex change in refractoriness, although the decrease in MAP was significantly greater. These results indicate that: (1) autonomic reflexes activated during acute myocardial ischemia shorten the refractory period of nonischemic ventricular myocardium; (2) the reflex response is predominantly mediated by enhancement of cardiac sympathetic nerve activity resulting from the reduced baroreceptor activity due to concurrent hypotension.

Animals↗
PubMed1982

Correlation between body surface isopotential maps and left ventriculograms in patients with old inferoposterior myocardial infarction.

In 24 patients with old inferoposterior myocardial infarction, body surface isopotential maps were compared with left ventriculographic findings. In 16 patients with asynergy restricted to the inferior and/or posterolateral segment, surface potential abnormalities due to infarction were observed during specific phases of QRS and in specific portions on the chest surface depending on the location and extent of ventricular severe asynergy (akinesis and dyskinesis). However, the remaining eight patients with coexisting severe asynergy in the anterior, apical, or septal segment showed surface potential maps quite different from those of the former patients. It is suggested that body surface isopotential maps are a useful clinical tool for detecting the location and extent of ventricular severe asynergy in patients with old inferoposterior myocardial infarction.

Aged↗
PubMed1981

Role of the conduction system in the endocardial excitation spread in the right ventricle.

The role of the Purkinje network in the excitation sequence in the endocardial surface of the right ventricle was studied using an isolated perfused canine preparation. The preparation was electrically stimulated at the proximal right bundle branch, and the activation time was mapped using contiguous bipolar electrodes or a microelectrode, or both. The earliest activation of muscle was observed at the junction between the ventricular septum and the free wall in front of the anterior papillary muscle. After the initial activation, the spread of ventricular muscle excitation in the free wall was essentially radial at a mean (+/- standard deviation) conduction velocity of 1.67 +/- 0.20 m/s. The activation of muscle in this area was almost always preceded by the activation of Purkinje fibers by 2 to 6 ms. Thus the Purkinje system was considered indispensable for the excitation spread in this area. In the lower third of the septum, the excitation sequence was essentially similar to that of the free wall, indicating a possible contribution of the fast conducting Purkinje system. In contrast, in the upper two thirds of the septum the activation of ventricular muscle spread from apex to base with a significantly delayed conduction velocity of 0.41 +/- 0.88 m/s, and it was not preceded by activation of Purkinje fibers, thus indicating the lack of involvement of the Purkinje system. Functional distribution of the anterior, posterior and lateral branches of the right bundle to the excitation spread of the right ventricular endocardial muscle was confirmed by the selective transection of one of these special conducting fibers, which suggested the etiologic significance of injury to each branch of the right bundle as a cause of various electrocardiographic patterns of incomplete right bundle branch block.

Action Potentials↗