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Biomedical subjects

I Kodama

Publications and source records attributed to I Kodama.

At least 217 records · Page 12Linked to original sources
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↗
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.

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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.

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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.

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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.

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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

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↗
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.

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PubMed1978

Effects of beta-adrenergic blocking drug pindolol (LB46) on cardiac fibers in relation to its membrane effects.

Direct membrane effects and beta-adrenergic blocking action of pindolol were studied comparatively on isolated perfused cardiac fibers of dogs. In Purkinje fibers, the duration of transmembrane action potential decreased in concentrations higher than 0.5 mg/L. Maximum rate of depolarization also decreased in higher concentrations (5.0 mg/L or more). The functional refractory period decreased to a lesser degree compared with the decrease of the action potential duration. Nevertheless, slow-rising action potentials could not be abolished in premature responses, probably because of membrane depressant effects of this drug. In ventricular muscle fibers, these changes were minimum in the same range of concentrations. On the other hand, 0.05 mg/L of pindolol which was close to the therapeutic plasma concentrations and had no effect on action potentials of both Purkinje and ventricular muscle fibers, minimized the increase in automaticity of Purkinje fibers induced by 0.2 mg/L of isoproterenol. It is rationally speculated that the mechanism of antiarrhthmic action of pindolol is mainly due to its beta-adrenergic blocking action.

Action Potentials↗
PubMed1978

Effects of l-penbutolol (Hoe 893d) on the transmembrane potentials of canine purkinje fibers and ventricular muscle fibers.

Intrinsic membrane effects (non-specific effects) and beta-adrenergic blocking action (specific effects) of l-penbutolol were studied using intracellular microelectrode techniques. l-Penbutolol in concentrations above 0.1 mg/L reduced the maximum rate of depolarization at phase O of both Purkinje fibers and ventricular muscle fibers without affecting their maximum diastolic potential. The action potential duration of Purkinje fibers were also shortened. The shortening of action potential duration and enhancement of automaticity in Purkinje fibers, normally induced by isoproterenol (0.2 mg/L), were antagonized by l-penbutolol in much lower concentraions (0.1--1.0 microgram/L) than those at which nonspecific effects are observed. The difference between these two concentration ranges is sufficient to suggest that l-penbutolol might be a highly specific beta-adrenergic blocking agent.

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