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Biomedical subjects

Y Nagamoto

Publications and source records attributed to Y Nagamoto.

12 recordsLinked to original sources
PubMed1992

Electrophysiologic changes before onset of ventricular tachyarrhythmias during partial reperfusion following severe myocardial ischemia in dogs.

We examined the electrophysiologic changes before an onset of ventricular tachyarrhythmia during partial reperfusion following severe myocardial ischemia. The left anterior descending coronary artery was occluded and cannulated below the occluded portion in 26 dogs. To deplete collateral flow into the ischemic myocardium, retrograde blood flow was induced for 20 min. Then, in all dogs except 7 with ventricular fibrillation during retrograde blood flow, partial reperfusion through collateral flow into the ischemic myocardium was produced by stopping the retrograde flow. Within 2 min of partial reperfusion, sustained ventricular tachycardia (VT) occurred in 7 dogs (group A) and non-sustained VT degenerating ventricular fibrillation occurred in 11 dogs (group B) of the remaining 12 dogs. In 6 dogs of group A and 9 of group B, epicardial conduction block appeared 5.0 +/- 2.2 and 3.5 +/- 1.3 min after ischemia. This was followed by fractionated electrical activities 15.2 +/- 3.2 and 11.7 +/- 3.3 min after ischemia. In group A, the fractionation had a slight change in configuration and a small increase in amplitude before the onset of VT during reperfusion; in group B, new deflections with large amplitude emerged before it. There was a significant difference in the amplitude (0.38 +/- 0.2 vs 0.67 +/- 0.3 mV, p < 0.025) between the 2 groups, although there was no significant difference in the amplitude (0.33 +/- 0.2 vs 0.23 +/- 0.1 mV) of the fractionation just before reperfusion. Our results show that slight improvement in fractionation induces sustained VT, and new deflections induce non-sustained VT degenerating ventricular fibrillation, even during partial reperfusion.

Animals↗
PubMed1992

Double atrial response to a single ventricular extrastimulus in a patient with Wolff-Parkinson-White syndrome.

Electrophysiological examination in a 39-year-old male disclosed an accessory pathway between the right atrium and the right ventricle and AV nodal dual pathways. Atrial and ventricular extrastimuli induced paroxysmal supraventricular tachycardia (PSVT), which was shown to be AV reciprocating tachycardia. Double atrial response was noted during ventricular extrastimuli at V1V2 of 280 msec and V1V2 of 250 msec. The first atrial response is considered to have been transmitted in a retrograde fashion in the accessory pathway, and the second atrial response similarly in the slow pathway of the AV node.

Adult↗
PubMed1991

Reflection as a cause of mid-systolic deceleration of pulmonary flow wave in dogs with acute pulmonary hypertension: comparison of pulmonary artery constriction with pulmonary embolisation.

STUDY OBJECTIVE: The aim was to examine whether mid-systolic deceleration of the pulmonary flow wave occurred in acute pulmonary hypertension due to pulmonary artery constriction and pulmonary embolisation, and if so whether it was related to reflection. DESIGN: Various degrees of pulmonary hypertension were induced by both pulmonary artery constriction and pulmonary embolisation in dogs. During control periods and during pulmonary artery constriction and pulmonary embolisation, pulmonary flow and pulmonary artery pressure were recorded, and the forward and backward (reflected) flow waves were separated from the measured pulmonary flow wave by the method of Westerhof et al. MATERIALS: 20 adult mongrel dogs were used and 10 dogs qualified for analysis. The other 10 dogs, which died before both interventions were completed, were excluded. MEASUREMENTS AND MAIN RESULTS: During pulmonary artery constriction, a distinct mid-systolic deceleration of the pulmonary flow wave was observed in five of the 10 dogs, while during pulmonary embolisation, no mid-systolic deceleration was found in these five dogs. The distinct deceleration of the pulmonary flow wave was related to a steep fall and early negative peak in the backward flow wave. CONCLUSION: Mid-systolic deceleration of pulmonary flow wave is likely to be related to reflection.

Acute Disease↗
PubMed1979

Electrophysiological actions of mexiletine (Kö1173) on canine Purkinje fibres and ventricular muscle.

1 The effects of mexiletine (Kö1173) were investigated in canine isolated cardiac Purkinje fibres and ventricular muscle with microelectrodes. Some Purkinje fibres were depolarized by mechanical stretch to induce spontaneous activity with slow upstroke velocity. The preparations were stimulated at rates of 1, 2, 3 and 4 Hz. The drug concentrations tested were 0.4, 2 and 10 mug/ml in Tyrode solution (KCl = 5.4 mM).2 The ;therapeutic' drug concentration (2 mug/ml) shortened action potential duration and effective refractory period of Purkinje fibres, the effect being pronounced at lower stimulation rates. In ventricular fibres, action potential duration changes were not consistent while the effective refractory period was prolonged.3 In depolarized Purkinje fibres showing automatic activity, the drug (0.4 or 2 mug/ml) depressed phase 4 depolarization and reduced the firing rate without changing maximum diastolic potential. However, when depolarized Purkinje fibres were electrically driven at a constant rate, the maximum diastolic potential became more negative with a concomitant decrease of pacemaker slope and increase of maximum rate of rise (V(max)) of action potentials.4 Moderate (2 mug/ml) to high (10 mug/ml) concentrations of the drug depressed V(max) in Purkinje fibres stimulated at 2 Hz by 12 and 42% respectively and depressed ;membrane responsiveness'. The decrease in V(max) depended upon the stimulation rate, being minimum at the lowest (1 Hz) and maximum at the highest (4 Hz) stimulation rate.5 The drug (2 mug/ml) improved V(max) of the earliest propagated premature action potentials by shifting the takeoff potential to more negative levels in both Purkinje and ventricular fibres.6 Membrane conductance in fibres mounted in a single sucrose gap chamber was increased by the drug (2 mug/ml) in both fibre types in normal and in Na(+)-deficient solutions. This increase was attributed to an increase in membrane K(+) permeability produced by the drug.7 All these effects are similar to those of lignocaine, diphenylhydantoin or aprindine, and can explain the antiarrhythmic action of mexiletine.

Animals↗
PubMed1977

Electrophysiologic effects of diltiazem, a new slow channel inhibitor, on canine cardiac fibers.

The effect of diltiazem hydrochloride (CRD-401), a coronary vasodilator, was investigated in isolated perfused canine ventricular muscles and Purkinje fibers using microelectrodes. The drug at a concentration of 1 microng/ml lowered the level of action potential plateau and shortened the duration in both ventricular and Purkinje fibers without change in maximum rate of rise (Vmax) or resting potential. Contractile tension of ventricular muscle was markedly decreased with shortening of plateau. With higher drug concentrations (5 microng/ml), Vmax in both ventricular muscle and Purkinje fiber decreased about 20% without change in resting potential, and the effect on repolarization became more marked. The drug blocked spontaneous firing which appeared in depolarized Purkinje fibers and abolished the automaticity elicited in electrically depolarized ventricular muscles. Input resistance of ventricular muscle, measured by small, hyperpolarizing short pulses, was not changed appreciably by the drug; suggesting no change in potassium conductance. These results suggest that the drug is a slow channel inhibitor, and its clinical implication is discussed in terms of antiarrhythmic activity.

Action Potentials↗
PubMed1976

Automaticity and time-dependent conduction disturbance produced in canine ventricular myocardium. New aspects for initiation of ventricular arrhythmias.

1) In isolated canine ventricular myocardium, automaticity could be induced by a passage of small depolarizing DC-currents. The mechanism was attributed to inflowing Ca++ and Na+ currents and time-dependent deactivation of outward K+ current under a condition of high membrane resistance due to an anomalous rectification. Significance of the automaticity was discussed in relation to the ventricular arrhythmias encountered in very early stage of myocardial infarction. 2) In in situ canine hearts, chloropromazine induced time (preceding cycle length)-dependent decrease in conduction velocity within the ventricle. Thus QRS-duration of non-premature beats was lenghtened at rapid pacing rates while QRS-duration of atrial premature beats was lengthened also at short coupling intervals in the drug-treated dogs. These slow conductions were not due to reduced take-off potential of action potentials bue due to drug-induced slow recovery of rapid Na+ system. The phenomenon may be responsible for reported QRS-prolongation and fatal ventricular arrhythmias encountered in the patients receiving phenothiazines.

Action Potentials↗
PubMed1976

Spontaneous electrical activity induced by depolarizing currents in canine ventricular myocardium. A preliminary note.

Spontaneous action potential (AP) discharge could be induced by an application of long (5-10 sec) depolarizing currents in 68% of canine ventricular myocardium tested in the voltage range between about -65 and -10 mV. The constant currents of various intensities were applied across a sucrose gap, and intracellular potentials were recorded with a microelectrode. The firing rate of the AP's was voltage-dependent and ranged between 0.7 and 2.5 Hz. The AP was dependent on both [Ca++]0 and [Na+]0. Increase of [Na+]0. Increase of [Na+]0 from 37 to 149 mM increased the firing rate, maximum rate of rise, and overshoot of the AP's while increase of [Ca++]0 from 0.45 mM to 1.8 and 7.2 mM increased the firing rate and maximum rate of rise, but did not change the amplitude of overshoot. AP discharges were not blocked by tetrodotoxin (10(-5) Gm/ml), but were effectively blocked by verapamil (6 X 10(-6) Gm/ml). Adrenaline (5 X 10(-6) Gm/ml) initiated AP's in otherwise quiescent preparations. The results suggest that spontaneous AP's may be produced by inflowing of slow Na+ and Ca++ currents modified by underlying change of K+-permeability. Possible clinical significance of this phenomenon is discussed in relation to ventricular arrhythmia.

Action Potentials↗
PubMed1976

The prolongation of QRS-duration resulting from delayed recovery of ventricular excitability. A new mechanism for intraventricular conduction disturbance. A preliminary note.

Chlorpromazine (1, 5, and 20 mg/Kg) was injected intravenously to anesthetized and open-chest dogs under artificial respiration. Using right atrial pacing, the heart rate was increased stepwise from intrinsic sinus rate to higher rate where the A-V block first developed. ECG (II) was recorded simultaneously with arterial blood pressure, ventricular monophasic action potentials and left atrial electrogram. In the control, QRS-duration was constant (46.9 +/- 0.8 msec) irrespective of heart rate. After the drug injection, however, the duration increased significantly with increasing heart rate, the effect depending on the injected dosage (r==0.283, P less than 0.1 in 1 mg/Kg; r==0.406, P less than 0.01 in t mg/Kg; r==0.631, P less than 0.001 in 20 mg/Kg). During the drug action, QRS-duration of atrial premature beats was also longer than that of sinus beats, and the lengthening increased with shortening of preceding cycle length. The observed QRS-prolongations were due to neither incomplete ventricular repolarization nor bundle branch block. The mechanism of prolongation was attributed to delayed or time-dependent recovery of ventricular excitability, i.e., slowed removal of inactivation in rapid sodium system in the ventricular muscle fibers.

Animals↗
PubMedDate not supplied

Electrically induced automaticity in canine ventricular myocardium.

Repetitive spontaneous action potentials (SAP) could be induced in canine ventricular and atrial muscle, although this inhibitory action was antagonized by the pretreatment with voltage range between about -60 mV and 0 mV. The SAP seemed dependent on both slow inward Ca2+ and Na+ currents and was suppressed by verapamil, Mn2+, and diltiazem, but not by tetrodotoxin. The increase of extracellular potassium concentration also suppressed the SAP. Acetylcholine could not block the SAP in ventricular muscle, but inhibited that in atrial muscle, although this inhibitory action was antagonized by the pretreatment with atropine. The automatic activity was attributed to slow inward Ca2+ and Na+ currents modified by decreasing time-dependent K+ outward current and K+ anomalous rectification.

Action Potentials↗
PubMedDate not supplied

Intraventricular conduction disturbance due to delayed recovery from ventricular inactivation in chlorpromazine-treated dogs.

In in situ canine hearts, chlorpromazine induced a time (preceding cycle length)-dependent decrease in conduction velocity within the ventricle. Thus, QRS duration of nonpremature beats was lengthened at rapid pacing rates while QRS duration of atrial premature beats was lengthened at short coupling intervals. These slow conductions were not due to reduced take-off potential of ventricular action potentials but to drug-induced slow recovery of the rapid Na+ system. The phenomenon may be responsible for reported QRS prolongation and fatal ventricular arrhythmias encountered in patients receiving phenothiazines.

Action Potentials↗