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Biomedical subjects

I Toda

Publications and source records attributed to I Toda.

At least 109 records · Page 6Linked to original sources
PubMed1990

Significance of Q wave disappearance in the chronic phase following transmural acute myocardial infarction.

The mechanism and prognostic implications of Q wave regression following transmural acute myocardial infarction (AMI) were assessed in 54 patients. Of these subjects, 14 lost their Q waves. Exercise myocardial thallium-201 (201Tl) scintigraphy and two-dimensional echocardiography were performed before the patients were discharged from hospital. Two-dimensional echocardiography and electrocardiography were simultaneously repeated about 18 months after AMI. Both the relative 201Tl activity in the infarcted area and the improvement of echocardiographic wall motion index were higher in patients who had lost their Q waves than in those with retained Q waves (70 +/- 14% vs 58 +/- 13%, p less than 0.01; 5.2 +/- 3.0 vs 2.0 +/- 3.4, p less than 0.01, respectively). The prevalence of post-infarction angina pectoris was significantly higher in the former (29% vs 0%, p less than 0.01). We concluded that remnants of viable myocardial muscle might be responsible for Q wave regression following transmural acute myocardial infarction, and the prevalence of post-infarction angina pectoris was high among these patients.

Adult↗
PubMed1990

Effects of a thromboxane A2 synthetase inhibitor on ventricular fibrillation threshold during coronary artery occlusion and reperfusion.

The effects of a new thromboxane A2 synthetase inhibitor (DP-1904) on electrical stability of the heart were tested in anesthetized, open chest dogs. The incidence of spontaneous ventricular arrhythmias, ventricular refractory period and ventricular fibrillation threshold (VFT) during ligation of the left anterior descending coronary artery (LAD) for 180 min and after reperfusion were measured as indices of stability. Ventricular fibrillation and ventricular tachycardia occurred spontaneously after ligation of LAD in 56% of 9 control dogs and 29% of 7 dogs which received intravenous DP-1904 (100 mg) before ligation of LAD (n.s.). In the control group, the ventricular refractory period decreased in the ischemic region; consequently, the difference in refractory period duration between the ischemic and non-ischemic regions (i.e., dispersion) increased 30 min after coronary ligation (7 +/- 9 ms vs 32 +/- 17 ms, p less than 0.05). The dispersion at 30 min after coronary ligation, though, was not affected in the DP-1904 treated group (2 +/- 4 ms vs 10 +/- 9 ms, n.s.). The VFT (determined with pulse trains) decreased from 28 +/- 5 mA to 15 +/- 11 mA (p less than 0.05) 30 min after coronary ligation in the control group, but was not affected (30 +/- 0 mA vs 27 +/- 4 mA) in the DP-1904 group. The plasma concentration of thromboxane B2 decreased after DP-1904 administration (baseline vs 30 min after coronary ligation: 475 +/- 165 pg/ml vs 165 +/- 74 pg/ml, n = 3, p less than 0.05), while the concentration of 6-keto-prostaglandin F1 alpha increased gradually. In conclusion, DP-1904 prevents a decline in electrical stability in the ischemic region of the canine heart during coronary occlusion.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Plastic injection method for preparing microvascular corrosion casts for SEM and its practical application.

This paper examines the application of the acryl plastic injection to the preparation of vascular corrosion microcasts for scanning electron microscopy (SEM). The original injection method using acryl plastic was described by Taniguchi, Ohta et al. in 1952 and 1955, under the title of "New improved method for injection of acrylic resin". Three dimensional observations were undertaken in our laboratory on the angiology at the macro- and microscopic levels of various organs from various mammals employing the original method. Based on this extensive experience, an injection method for preparing corrosion microcasts for use in SEM was devised in our laboratory. Microcasts prepared by the present method were able to demonstrate the fine vascular architecture of each organ. In general, although applications for preparing vascular microcasts of isolated and parenchymal organs are not so difficult, the method can be used to be applicable for demonstrating the fine vascular architecture related to or within hard tissues, as well as for investigating the morphological relations between changes of vascular patterns and restorative changes in the surrounding tissues affected by experimental operations. SEM microphotographs are also presented to illustrate actual practical applications.

Animals↗
PubMed1989

Evaluation of antifibrillatory effects of drugs.

Several electrical stimulation techniques have been used to measure ventricular fibrillation (VF) threshold such as single pulse stimulation, train of pulses stimulation, continuous 50-Hz stimulation and sequential pulse stimulation. This study was undertaken to clarify the difference in VF threshold values obtained by each method. The development of VF was classified into 4 stages. Stage 1 is the phase in which fragmented activities are generated at the stimulated area of the ventricular muscle. In stage 2, the local activities propagate to surrounding ventricular muscle, causing ventricular excitation. Stage 3 is characterized by repetitive ventricular excitations. In state 4, repetitive ventricular responses in a form of accelerating tachycardia induce disorganized excitations that finally degenerate into fibrillation. Based on this classification of stages between local excitation and fibrillation, single pulse stimulation is considered to measure VF threshold for stages 1 to 4, continuous 50-Hz stimulation for stages 2 to 4 and sequential pulse stimulation for stages 3 and 4. Thus, the antifibrillatory effect of drugs can be interpreted with some significance by using different stimulation methods. The sequential pulse stimulation method revealed that some antiarrhythmic agents caused a dissociation between repetitive nonstimulated excitation (RE) threshold and VF threshold. Procainamide and disopyramide increased RE threshold while decreasing VF threshold. Mexiletine and lidocaine elevated both RE and VF thresholds. Local infusion of procainamide at the site of test stimulation reduced both thresholds. However, after the application of procainamide to the whole heart, RE threshold remained decreased but VF threshold was elevated. It is likely that the antifibrillatory effect of the drug includes 2 different processes: antireentrant and antimultiple reentrant effects.

Animals↗
PubMed1989

Further observations on entrainment of atrial flutter in the dog.

To determine whether the first postpacing interval after entrainment was affected by recording and pacing sites, overdrive atrial pacing was undertaken in 13 episodes of atrial flutter with a mean flutter cycle length (FCL) of 140 +/- 8 msec induced in seven dogs. Atrial flutter was induced by means of an anatomic obstacle. Seven recording sites, four in the right atrium and three in the left atrium, and three pacing sites, two in the right atrium and one in the left atrium, were selected. After entrainment from the right atrium at pacing cycle lengths that were 94% of the FCL, the first postpacing interval was not significantly different from the intrinsic FCL at each recording site, but it tended to be shorter than the FCL at the recording sites near pacing sites. For entrainment from the left atrium, the first postpacing interval was longer than the FCL at recording sites in the left atrium (p less than 0.001), but it was not different from the FCL at recording sites in the right atrium. These results are due to differences in placement of recording and pacing electrodes relative to the reentrant circuit. Also we observed that activation sequences involving three appropriately selected recording sites were always identical when paced from two different pacing sites at a single constant pacing cycle length. This new phenomenon may best be explained by postulating reentry as the mechanism for atrial flutter.

Animals↗
PubMed1989

Summation and inhibition by ultrarapid train pulses in dogs: effects of frequency and duration of trains, lidocaine, and beta blockade.

To test whether summation and inhibition of excitation by ultrarapid train pulses were modified by frequency and duration of trains, using lidocaine and beta blockade, the strength-interval relationship was determined with a single extrastimulus and train pulses (100 and 200 Hz) in 28 anesthetized, open-chest dogs. The effective refractory period (ERP) determined at greater than or equal to 5 mA was shorter for trains than for single stimulus (summation). Summation determined at 15 mA increased progressively as the duration of trains was increased to 50 msec after which it reached a plateau. ERP determined at less than or equal to 2 mA was longer with train pulses than with single stimulus (inhibition). Inhibition for 200 Hz trains increased linearly with train duration up to 200 msec, while for 100 Hz trains it became constant when the duration was greater than or equal to 80 msec. Lidocaine (plasma concentration: 2.6 +/- 1.0 micrograms/mL) did not affect inhibition and summation in 11 dogs. Propranolol (1 mg/kg, iv) increased summation at 15 mA (n = 7, 30 +/- 10 vs 46 +/- 11 msec with 100 Hz trains, P less than 0.01), but did not affect inhibition (37 +/- 26 vs 29 +/- 17 msec, NS). In conclusion, (1) effect of frequency of train pulses was more on inhibition than on summation; (2) lidocaine did not affect inhibition and summation; and (3) propranolol increased summation but not inhibition.

Adrenergic beta-Antagonists↗
PubMed1989

Electrophysiological study of young patients with exercise related paroxysms of palpitation: role of atropine and isoprenaline for initiation of supraventricular tachycardia.

Electrophysiological studies were performed in eight patients (four men and four women, mean (SD) age 24 (5) years with paroxysmal attacks of palpitation during or immediately after exercise. Five patients were competitive athletes at college. In two patients spontaneous supraventricular tachycardia during exercise was recorded by ambulatory electrocardiographic monitoring and in another it was induced by treadmill exercise testing. Two had dual atrioventricular nodal pathways, three had manifest atrioventricular accessory pathways, and three had concealed atrioventricular pathways. Programmed stimulation induced sustained supraventricular tachycardia in six patients--in two after intravenous injection of atropine sulphate (1 mg) and in four during infusion of isoprenaline (0.01 microgram/kg/min). In one patient, non-sustained atrioventricular nodal reentrant tachycardia was induced during isoprenaline infusion. In the remaining patient, who had dual atrioventricular nodal pathways, tachycardia was not inducible. AH block prevented maintenance of reentry in five patients. In five patients shortening of the effective refractory period of the atrioventricular node with atropine (one patient) and isoprenaline (four patients) caused sustained supraventricular tachycardia. The present study indicates that treatment with atropine and isoprenaline may be an important factor in the initiation of supraventricular tachycardia in patients with exercise related paroxysms of palpitation.

Adult↗
PubMed1989

Effects of antiarrhythmic drugs on the repetitive extrasystole threshold and the ventricular fibrillation threshold.

The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.

Animals↗
PubMed1989

[Objective examination and diagnosis of bruxism. 1. New device for recording muscle activity and tooth contacts during sleeping at home].

The purpose of this study was to make an objective diagnosis of bruxism using a new recording system by observation during sleeping at home. The system was composed of a portable recorder for monitoring bruxism at home and an analyzing device for recalling the data later in laboratory. Muscle activity as recorded by EMG, occlusal tooth contacts were monitored by microvibration pick-up, and grinding sounds were recorded by a small microphone, simultaneously. These were printed on the one recording paper by playing back the tape. Six subjects were selected and were monitored individually for five nights with this new system at home. Records were transcribed and analyzed in the laboratory. As a result, nocturnal muscle activity, occlusal tooth contacts, and grinding sounds were recorded and analyzed efficiently with system. This new system is considered in useful for the investigation and diagnosis of bruxism in periodontal disease.

Bruxism↗
PubMed1989

[Cardiac response during various activities in patients with ischemic heart disease evaluated by an ambulatory ventricular monitor (VEST)].

To assess the cardiac response to various exercise in ischemic heart disease (IHD), left ventricular function was continuously measured with an ambulatory ventricular monitor (VEST) in 3 normal subjects and 15 IHD patients. Treadmill exercise (early stage (E1), end stage (E2) and recovery standing state (RE], walking (WK) and climbing stairs (CS), was used for exercise. 15 IHD patients were divided into 4 groups by the LVEF response to treadmill exercise. In group 1 (G1), LVEF increased gradually at stage 1 and became plateau from stage 2 to end stage like normal group. In group 2 (G2), LVEF increased at stage 1 and became plateau from stage 2 but decreased from maximal EF more than 5% at end stage. In group 3 (G3), LVEF increased only at stage 1 and decreased immediately after stage 1 to end stage. The decrease of LVEF at end stage from standing was more than 5%. In group 4 (G4), LVEF decreased at stage 1 and became minimum at end stage. This grouping was well related to thallium redistribution (Tl RD) score and coronary arteriography (CAG) score. We could predict the severity of coronary artery disease from this grouping because all group 3 or 4 patients had severe coronary artery disease. VEST was useful for the evaluation for the tolerance to daily activities. Group 1, 2 and 3 tolerated daily activities while group 4 could not always. The degree of the increase in cardiac output during ischemia evaluated by VEST may be one of the useful index of the tolerance to exercise. In conclusion VEST was very useful for evaluating cardiac capacity of ischemic heart disease patients during various exercise.

Coronary Disease↗
PubMed1988

ST-T isointegral analysis of exercise stress body surface mapping for identifying ischemic areas in patients with angina pectoris.

ST-T isointegral analysis of body surface mapping was used in an attempt to localize ischemic areas on exercise tests. In 28 patients with angina pectoris and 10 healthy subjects, body surface potential was recorded with 87 leads, and ST isopotential and ST-T isointegral maps were constructed. In all 10 healthy subjects, the basic pattern of the ST-T isointegral map showed no significant change after exercise. In 23 of 28 patients with angina pectoris (82%), alterations in the ST-T isointegral map after exercise were observed. They were divided into four types (anterior, inferoposterior, lateral, and global) according to the distribution of negative values, which were well correlated with the extent of ischemic area determined by thallium myocardial scintigraphy and coronary angiography. The postexercise ST-T isointegral map was normalized after administration of nitroglycerin in four of five patients. In five patients (18%) who did not show abnormalities on the postexercise ST-T isointegral map, the magnitude of maximal ST depression was significantly smaller than that observed in the other 23 patients with angina pectoris (0.14 vs 0.23 mV on the average, p less than 0.05). It was concluded that the exercise test with ST-T isointegral mapping is a new method for noninvasive detection of location and severity of ischemic regions.

Adult↗
PubMed1988

Epicardial mapping of polymorphous ventricular tachycardias induced in the canine heart with procainamide.

To elucidate the mechanisms of the arrhythmogenic and antifibrillatory action of procainamide, 24 episodes of polymorphous ventricular tachycardia were analyzed. They were induced electrically in 12 canine hearts before and after the administration of 40 mg/kg of procainamide. The isochronal maps of the epicardial activation sequence were successfully constructed by 40 simultaneously recorded bipolar electrograms in 14 of 17 episodes after procainamide. The isochronal maps showed a possible macroreentrant circuit in 12 episodes, and in four of them the functional block was noticed to have disappeared before the termination of tachycardia. This study suggests that procainamide predisposes the ventricle to reentrant tachyarrhythmias and that the dimension of the reentrant circuit induced is too large to be fragmented into multiple reentries, which results in the prevention of the development of ventricular fibrillation.

Animals↗
PubMed1988

Ventricular fibrillation threshold measured by continuous 50 cps stimulation for the evaluation of the antifibrillatory effect of the drugs.

The role of electrophysiologic parameters on the induction of ventricular fibrillation (VF) by continuous 50 cycle per second (cps) electrical stimulation was studied in 21 open chest dogs. The current strength of the 50 cps stimulation required to induce VF when applied to the ventricle for 2 seconds was defined as the ventricular fibrillation threshold (VFT). The intravenous injection of antiarrhythmic drugs raised the VFT in a dose dependent manner. The changes in VFT were associated with a rise in excitation threshold. The slopes of the regression equations relating the excitation threshold to VFT were almost identical, that is, 2.8 with lidocaine, 3.4 with procainamide and 3.2 with disopyramide. Prolongation of refractory period increased the cycle length of ventricular excitations just prior to VF but was not correlated with the changes in VF. Localized myocardial ischemia induced by coronary ligation also resulted in the elevation of VFT. The slope of the regression equation between excitation threshold and VFT was 1.9 which was slightly lower than that observed at the administration of the drugs. The fact that the VFT was mainly attributed to the changes in excitation threshold at the site where the test stimulus was applied would limit the usefulness of the 50 cps continuous stimulation method for the evaluation of vulnerability to VF.

Animals↗
PubMed1987

Plasma concentration of atrial natriuretic polypeptide in patients with atrial tachycardia.

To investigate the mechanisms of polyuria associated with tachycardia, we measured plasma concentrations of alpha-human atrial natriuretic polypeptide (alpha-hANP) and cGMP in 6 patients with paroxysmal tachycardia. Plasma concentrations of immunoreactive alpha-hANP and cGMP increased by +69% (p less than 0.05) and +100% (p less than 0.05), respectively, during both paroxysmal atrial tachycardia and atrial fibrillation. To examine whether tachycardia per se raises the secretion of alpha-hANP, we also determined plasma concentrations of alpha-hANP and cGMP in 5 patients during rapid atrial pacing. The pacing-induced tachycardia also increased both of the plasma concentrations. Further, the examinations of cardiac and renal functions in patients with complete atrioventricular block during rapid pacing revealed that each of the increases in atrial pressures, urinary sodium excretion and creatinine clearance were in parallel with the change in plasma concentration of alpha-hANP. These results suggest that an increase in plasma concentration of alpha-hANP during paroxysmal tachycardia is mainly due to elevation of atrial pressure and that this increase in alpha-hANP contributes to tachycardia polyuria.

Atrial Fibrillation↗
PubMed1986

Epicardial activation patterns of torsade de pointes in canine hearts with quinidine-induced long QT interval but without myocardial infarction.

We studied the epicardial activation sequence during torsade de pointes in canine hearts with quinidine-induced long QT interval. Following a toxic dose of quinidine sulfate (30 mg/kg), polymorphic ventricular tachycardia was induced by extrastimuli. In nine dogs, 22 episodes of nonsustained polymorphic ventricular tachycardia and six episodes of monomorphic ventricular tachycardia were induced. Of 22 episodes of nonsustained polymorphic ventricular tachycardia, 12 episodes showed typical torsion of the spikes of the QRS complex around the isoelectric line (torsade de pointes). Isochronal maps were made from 38 simultaneously recorded bipolar electrograms and showed that each change in QRS morphology was associated with a change in the earliest epicardial activation site and/or a change of epicardial activation sequence. During episodes of torsade de pointes, the earliest epicardial activation site migrated gradually from one site to another site. The transitional QRS complexes had their earliest epicardial activation sites between the new and old site of the earliest epicardial activation. The changes in the earliest epicardial activation site during polymorphic ventricular tachycardia without torsade de pointes pattern was not as great as that noted during torsade de pointes. This study suggests that in a noninfarcted canine model torsade de pointes is produced by alteration in the earliest site of activation rather than by competition from two or more competing foci.

Animals↗