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Biomedical subjects

J Toyama

Publications and source records attributed to J Toyama.

At least 181 records · Page 10Linked to original sources
PubMed1981

Electromechanical effects of anthopleurin-A (AP-A) on rabbit ventricular muscle: influence of driving frequency, calcium antagonists, tetrodotoxin, lidocaine and ryanodine.

1 Anthopleurin-A (AP-A 5 x 10(-9) M, 1 x 10(-8) M) caused a prolongation of action potential duration (APD) and an increase of contractile force in rabbit isolated ventricular muscle preparations.2 The prolongation of APD and the positive inotropic effect of AP-A (1 x 10(-8) M) were augmented by lowering the driving frequency from 2.0 to 0.2 Hz, resulting in an apparent negative staircase of contractile force in this frequency range. When the preparation was driven at an extremely low frequency (0.017 Hz), AP-A did not increase the contractile force, but caused a considerable prolongation of APD.3 Verapamil (1 x 10(-6) M) and nifedipine (1 x 10(-6) M) had no apparent influence on the APD prolongation by AP-A (5 x 10(-9) M, 1 x 10(-8) M). The positive inotropic effect of AP-A was also relatively well maintained even in the presence of these calcium antagonistic drugs when the preparation was driven at a lower frequency (0.2 Hz).4 Tetrodotoxin (TTX 2 x 10(-6) M) and lidocaine (1 x 10(-4) M) markedly inhibited both the APD prolongation and the positive inotropic effect of AP-A (1 x 10(-8) M).5 In the presence of ryanodine (2 x 10(-6) M), an agent which is known to interfere with calcium release from the intracellular activator pool, AP-A (1 x 10(-8) M) failed to cause its positive inotropic effect in spite of the marked prolongation of APD.6 These results suggest that the effects of AP-A on cardiac muscle are primarily mediated by the fast sodium inward current. Thus, delayed inactivation of sodium inward current may cause APD prolongation, and probably induces an alteration of intracellular calcium kinetics reflected by an increase of contractile force.

Action Potentials↗
PubMed1981

Effect of ouabain on electrical coupling of rabbit atrial muscle fibers.

The effects of ouabain on passive electrical properties of isolated rabbit atrial muscle fibers (crista-terminalis) were investigated. The space constant as well as the time constant of the crista-terminalis was determined using the partition method of Kamiyama and Matsuda based on the cable equation proposed by Hodgkin and Rushton. Ouabain treatment for 30 minutes at a lower concentration (2 X 10(-7) M), caused no significant change in the space constant and time constant of the crista-terminalis. After ouabain treatment for 30 minutes at a higher concentration (1 X 10(-6) M), the space constant of the crista-terminalis was reduced significantly, whereas the time constant was not affected. An apparent reduction in the resting membrane potential and the amplitude of action potential was also observed at the higher concentration of ouabain. These effects of ouabain on passive electrical properties of the crista-terminalis are most likely explained by the increase of its axial resistance (electrical uncoupling) due to intracellular calcium accumulation resulting from inhibition of the membrane sodium pump. This suggests that such an electrical uncoupling may play an important role in the intra-atrial conduction disturbance by cardiac glycosides.

Action Potentials↗
PubMed1981

Effects of injury to the right ventricular conducting tissue of canine hearts on epicardial activation sequence and electrocardiograms.

The distal right ventricular conducting tissues of 45 canine hearts were experimentally interrupted in various degrees by a transmural incision of the right ventricular free wall, a trans-section of the lateral branches of the right bundle or by injury to the endocardial Purkinje network. Right ventriculotomy caused a slight activation delay (less than 10 msec) of the right ventricle which was restricted to the distal area from the incision, but the delay was not long enough to cause a significant prolongation of the QRS duration in the limb lead ECG. In one experiment, a vertical incision in the middle region induced an exceptional, marked alteration of the right ventricular activation sequence and an apparent prolongation of the QRS duration (16 msec) indicating an incomplete RBBB. However, anatomical analysis revealed that the lateral branches were nearly completely interrupted by the incision. An extensive injury to the Purkinje network extending toward the right ventricular outflow tract by a blunt scalpel caused a local activation delay in the outflow tract, without producing any serious delay resulting in an ECG pattern of RBBB. These results may suggest that right ventriculotomy would induce the RBBB pattern of ECG if lateral branches are extensively injured by the surgical procedure, and that the injury to the Purkinje network extending toward the outflow tract does not play a primary role of genesis of RBBB pattern in ECG.

Action Potentials↗
PubMed1981

Body surface isopotential maps of experimentally induced transient right bundle branch block.

The characteristic patterns of the epicardial activation and body surface isopotential maps (MAPs) were examined in experimental transient right bundle branch block (RBBB) produced by pressing the main stem of right bundle mechanically. During the recovery from the complete block, various degrees of incomplete RBBB (IRBBB) were obtained. The epicardial activation of IRBBB spread in almost normal fashion with delayed right ventricular epicardial breakthrough. And the MAPs manifested intermediate patterns between those obtained in control and in complete RBBB (CRBBB). The MAP patterns of IRBBB were classified into the following 3 groups by the difference of the localized bend of isopotential lines reflecting the epicardial breakthrough. In the advanced IRBBB with QRS prolongation over 25%, the epicardial breakthrough of the left ventricle was detected on the MAPs. In the moderate IRBBB with QRS prolongation around 20%, in addition to the left ventricular breakthrough the right ventricular breakthrough was detected at the center of the anterior chest. In the mild IRBBB with QRS prolongation less than 15%, only the right ventricular breakthrough was detected. These findings indicate usefulness of MAPs for diagnosing the severity of IRBBB due to the damage to the main right bundle. Moreover, these MAP patterns in IRBBB of main right bundle can be distinctly differentiated from the IRBBB MAPs resulting from incisional interruption of lateral branches of right bundle. The present findings also suggest the usefulness of MAPs in diagnosing the site of the conduction disturbance resulting in IRBBB.

Animals↗
PubMed1981

Recognition of the epicardial breakthrough on body surface isopotential maps: influence of the inter-electrode distance on the patterns reflecting the epicardial breakthrough.

The epicardial breakthrough can be recognized from the localized depression of the body surface potential, which is characterized by a localized bend of the equipotential lines or a send-minimum on isopotential maps. Recognition of epicardial breakthrough with isopotential maps enables us to diagnose location of the block site of the bundle branch blocks more precisely than by ECG or VCG. However, the optimum inter-electrode distance for detection of such a localized potential has not been determined. In the present study, influence of the inter-electrode distance on the characteristic patterns reflecting the epicardial breakthrough was studied on 16 healthy persons using 9 x 9 electrode arrays with inter-electrode distance of 1.25 cm, 5 x 5 with 2.5 cm, and 3 x 3 with 5 cm. Breakthrough was recognized in 15 out of 16 cases (94%) on maps recorded with electrode arrays with inter-electrode distance of 1.25 and 2.5 cm. However, detectability of the breakthrough was reduced to 10 out of 16 cases (63%) with electrode array having inter-electrode distance of 5 cm. In conclusion, it is preferable to use an electrode array with an inter-electrode distance of no more than 2.5 cm for the purpose of breakthrough recognition.

Adult↗
PubMed1981

Effects of high frequency stimulation on the membrane potential of isolated ventricular muscle and Purkinje fibers.

Effects of high frequency (HF) stimulation on membrane potential were examined in ventricular muscle and Purkinje fibers, which were isolated from canine and rabbit hearts, by using microelectrode techniques. When the stimulating frequency of preparations was increased abruptly from basic frequency (BF, 0-30/min) to high frequency (HF, 60-150/min), the maximum diastolic potential (MDP) of both ventricular muscle and Purkinje fibers decreased with each beat and reached a minimal value (initial depolarization). Then, MDP gradually increased beyond the steady state level at BF (hyperpolarization). On returning the stimulating frequency from HF to BF, a further terminal hyperpolarization ensued, and finally MDP decayed back (both depolarization and hyperpolarization) was apparently greater in ventricular muscle than in Purkinje fibers. A significant increase of threshold current for excitation and a slight increase of membrane input resistance were also observed at the hyperpolarized period after HF stimulation. Lowering the temperature of the perfusate from 37 degrees C (control) to 31 degrees C or 26 degrees C led to an augmentation of initial depolarization and also a decrease in the intensity of ensuing hyperpolarization. The decay time of the hyperpolarization after HF stimulation was much prolonged. In the presence of ouabain, HF stimulation caused a monotonic decline in MDP and no hyperpolarization was recorded during and after HF stimulation. These results suggest that an active ion transport through the sodium pump contributes significantly to the electrical properties of ventricular muscle as well as the Purkinje fibers when the firing rate of the fibers is abruptly changed.

Animals↗
PubMed1981

Experimental appraisal for diagnosis of right bundle branch block using the body surface isopotential maps.

This study was designed to detect reflection of epicardial breakthrough to body surface isopotential maps by recording epicardial and body surface maps simultaneously, and to estimate changes in epicardial breakthrough associated with complete and incomplete blocks induced by compression of the main stem of the right bundle branch of trans-sectioning of the lateral branches. In the control, epicardial breakthrough appearing on the right ventricular surface was well detected on the body surface maps as a bend of isopotential lines localized at the mid sternum at 11.5 +/- 1.6 msec (n = 5) after QRS initiation. At complete block immediately after compression of the main stem, the localized bend shifted inferiorly to the left at 17.8 +/- 1.8 msec (n = 5) after QRS initiation, suggesting appearance of the left ventricular epicardial breakthrough. With progression of recovery from the compression, in addition to epicardial breakthrough on the left ventricle, the breakthrough on the right ventricle became detectable again with a delay of 5 msec, and then the former was faded away as time progressed. After trans-sectioning of the lateral branches, sequential changes in the body surface maps were almost the same as in complete block of the main stem but they lapsed about 43 msec (n = 5) shorter in comparison with the complete block. In conclusion, detection of the localized bend of the isopotential lines on the body surface can provide diagnosis of the site and degree of the right bundle branch block in detail.

Animals↗
PubMed1981

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

In 30 patients with old anterior myocardial infarction, body surface isopotential maps were correlatively studied with left ventriculographic findings. In 25 patients with ventricular asynergy restricted to the anterior segments, surface potential abnormalities due to infarction were observed during specific phases of QRS and in specific portions of the chest surface depending on the location and extent of severe ventricular asynergy (akinesis and dyskinesis). However, the remaining 5 patients with co-existing severe asynergy in the inferoposterior segment, showed body surface potential maps quite different from those of the above 25 patients. It was suggested that body surface isopotential maps were useful in detecting the location and extent of ventricular severe asynergy in patients with old anterior myocardial infarction.

Adult↗
PubMed1980

Effects of hypoxia or low PH on the alternation of canine ventricular action potentials following an abrupt increase in driving rate.

Effects of hypoxia or low extracellular pH on the alternation of ventricular action potentials occurring after an abrupt increase in driving rate (rate change induced alternation--RCI alternation) were studied using standard microelectrode methods in canine papillary muscle preparations. Under the control conditions the alternation always occurred after a rate change from 10 to 100 beats . min-1 or 60 to 200 beats . min-1, but it diminished rapidly during the faster rates. Under the hypoxic condition the degree of the RCI alternation gradually increased to the peak 20 to 60 min after the onset of the hypoxic perfusion and then decreased. The hypoxic perfusion caused an increase in beat-to-beat laternating change of the action potential configuration and a marked persistence of the phenomenon. In the initial stage of reoxygenation after 2 hours of the hypoxic perfusion, the RCI alternation transiently increased again. During hypoxia in six out of 15 preparations an unusual alternation of action potentials with an inverted phase occasionally occurred after the rate change from 60 to 200 beats . min-1. Acidic perfusion (pH = 6.0) had similar effects on the RCI alternation. It also caused an increase in beat-to-beat alternating change in the action potential configuration and a prolongation of the phenomenon. In the period when the RCI alternation was markedly increased, a steady-state alternation of action potentials spontaneously occurred at a constant drive rate under hypoxia or low pH. The mechanisms responsible for the RCI alternation of action potentials and the possible role of the phenomenon in the genesis of cardiac arrhythmias in the ischaemic heart are discussed.

Action Potentials↗
PubMed1980

Effects of niludipine (Bay-a-7168) on transmembrane action potentials of rabbit sinus node cells and atrial muscle fibers.

Effects of niludipine (bis(2-propoxyethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedic arboxylate; Bay-a-7168) on isolated rabbit sinus node and right atrial preparations were studied using intracellular microelectrode techniques. Niludipine in concentrations above 1 X 10(-8) M caused dose-dependent changes in the membrane action potentials of the preparations. In spontaneously firing sinus node cells, a marked decrease in the amplitude (AMP) and maximum rate of depolarization (MRD) of action potentials as well as a slight decrease in their maximum diastolic potential (MDP) were observed after drug administration. In constantly driven atrial muscle fibers, the early repolarizing phase was accelerated (shortening of action potential duration) and AMP was decreased by several millivolts. However, little change occurred in the MDP and MRD of atrial muscle fibers even at the highest concentration (1 X 10(-6) M). Niludipine prolonged the effective refractory period of atrial muscle fibers by 4--8 msec. At the same time, it caused a marked decrease in the amplitude of the premature action potentials and prolonged their propagation time. Most of these effects of niludipine, which may be attributed to the reduction of the slow inward current through the myocardial cell membrane, were antagonized by the concomitant administration of isoproterenol (1 X 10(-6) M).

Action Potentials↗
PubMed1980

Effects of rapid stimulation on the transmembrane action potentials of rabbit sinus node pacemaker cells.

We studied the mechanism of post-overdrive suppression in superfused rabbit sinus node pacemaker cells. Small specimens of sinus node tissue isolated from rabbit hearts were driven at a fast rate (overdrive) for 10-120 seconds using single sucrose gap methods. During the control perfusion (35 degrees C Tyrode's solution), overdrive caused a progressive decrease in maximum diastolic potential (MDP), overshoot (OS), and maximum rate of depolarization at phase 0 [dV/dt)max]. After cessation of the overdrive, the rate of diastolic depolarization decreased, and the spontaneous activity was suppressed temporarily (post-overdrive suppression). MDP, OS, (dV/dt)max, and the spontaneous activity returned within a few seconds to the level observed before overdrive. Atropine (2 x 10(-6) g/ml) did not influence the effects of overdrive. After ouabain administration (3 x 10(-7) g/ml) or in low temperature perfusate (25 degrees C), the effects of overdrive were accentuated, and a marked suppression of spontaneous activity with a long pause of over several seconds was seen following the overdrive. These results suggest that the post-overdrive suppression of sinus node is attributable, at least in part, to ionic shifts following overdrive, and may be potentiated by metabolic dysfunction of pacemaker cells.

Action Potentials↗
PubMed1980

The body surface isopotential maps of the non-transmural infarctions--a simulation study of excitation spread in a ventricular model.

Simulation by a digital computer of excitation spread in a human ventricular model produced displays of body surface isopotential maps. Localization of model myocardial infarctions to non-transmural and transmural sites produced distinctive differences in these displayed isopotential maps. The body surface directly over the infarcted lesion was negative in potential only in the first half period of the QRS complex and then became positive. The model demonstrated that this later positive potential was due to delayed arrival of excitation to the subepicardial layer outside of the subendocardial lesion. While, in transmural infarction, the overlying body surface remained negative in potential throughout the QRS complex. It is expected that body surface isopotential maps will become clinically available and will permit helpful differential diagnoses between non-transumral and transmural myocardial infarctions.

Computers↗