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Biomedical subjects

T Tamamura

Publications and source records attributed to T Tamamura.

36 records · Page 2Linked to original sources
PubMed1990

Left ventricular filling pattern in congestive heart failure patients with normal sinus rhythm--a decreased ratio of peak mitral flow velocity in atrial systole relative to that in early diastole may reflect markedly increased left ventricular end-diastolic pressure.

The left ventricular filling pattern was studied by pulsed Doppler echocardiography in 13 congestive heart failure patients with normal sinus rhythm. The first study was done when congestive heart failure was present; the second after the signs and symptoms of congestive heart failure disappeared. In 12 of the 13 patients, the peak mitral flow velocity in atrial systole (PFVA) increased after the congestive heart failure disappeared (mean increase from 50.5 cm/sec to 74.8 cm/sec : p = 0.0001, paired t test), and the peak mitral flow velocity in early diastole (PFVE) decreased significantly in all 8 patients in whom secondary mitral regurgitation became less severe after improvement of congestive heart failure (mean decrease from 90.8 cm/sec to 52.0 cm/sec : p = 0.0001, paired t test). The ratio of PFVA to PFVE (PFVA/PFVE) increased in all cases after the congestive heart failure improved (mean increase from 0.59 to 1.33 : p = 0.0001, paired t test). The PFVA/PFVE is a simple index of left ventricular diastolic function. A PFVA/PFVE greater than one indicates disturbed left ventricular diastolic function. However, when the PFVA/PFVE is in a normal range for the patients' age ("pseudo-normalization") and is accompanied by impaired left ventricular systolic function in congestive heart failure, markedly increased left ventricular end-diastolic pressure must be considered.

Adult↗
PubMed1990

[Congestive heart failure in the elderly: severe tricuspid regurgitation by two-dimensional Doppler echocardiography].

We studied five cases of atrial fibrillation in the elderly showing severely decreased exercise tolerance (NYHA III) and normal left ventricular function. There were no signs of classical tricuspid regurgitation. Both atria were enlarged and right ventricular sizes were shown by two-dimensional echocardiography to have mildly increased. Two-dimensional Doppler echocardiography revealed severe tricupid regurgitation but at a maximal velocity less than 2.3 m/sec, meaning that right ventricular pressure was not increased. Cardiac output (CO) and circulating blood volume (BV), measured by radiocardiography showed CO to have decreased and BV to have increased. No intracardiac shunt was detected. The cause of this decreased exercise tolerance in the group in our study is thought to be right ventricular dysfunction due to the aging process. This also occurs in a similar pattern in younger people who have arrhythmogenic right ventricular dysplasia (ARVD), Uhl's disease, or right ventricular dilated cardiomyopathy.

Aged↗
PubMed1989

Combined effect of disopyramide and bethanechol: use of bethanechol to prevent anticholinergic side effects of disopyramide without reduction of antiarrhythmic efficacy.

Because bethanechol chloride (B) relieves the anticholinergic side effects of disopyramide (D), we examined the combined effects of D and B on the heart and urinary bladder. B was confirmed to counteract dose dependently the effect of D on the dog bladder. In the ventricular muscle, the combined electrophysiological effects (D + B) were additive, with no reduction in the effect of D. With the control value set as 100%, the decrease in the maximum rate of depolarization with 5 X 10(-6) g/ml D (90 +/- 6%) was not affected by the same dose of B (D + B: 84 +/- 14%). Moreover, the effective refractory period (ERP) was larger with D + B (128 +/- 12%) than with either B (109 +/- 9%, p less than 0.01) or D (115 +/- 11%, p less than 0.05). In contrast, in the atrial muscle and AV and SA nodes, B had marked acetylcholine-like effects. These were completely suppressed by the addition of D except for the atrial ERP with the highest tested concentration of B (5 X 10(-6) g/ml). In the latter case, the prolongation of ERP was minimal (B + D: 105 +/- 14%) as compared with D alone (130 +/- 15%). Since the plasma concentration of B after oral administration of a clinical dose is expected to be on the order of 10(-7) g/ml, no practical effect is anticipated. We conclude that B can be expected to counteract urination disorders caused by D without reducing D's antiarrhythmic efficacy.

Anesthesia↗
PubMed1988

Terpentecin, an inhibitor of DNA synthesis.

Terpentecin at a concentration of 0.78 microgram/ml decreased the number of viable cells of Escherichia coli NIHJ to less than one thousandth the starting number in an hour when added to an exponentially growing culture in a nutrient broth. During this time, the turbidity of the cell suspension kept increasing as fast as the control. Microscopic inspection of the cells exposed to terpentecin under these conditions revealed that the cells were elongated. Terpentecin at a concentration of 6.25 micrograms/ml inhibited incorporation of [14C]thymidine into the acid-insoluble material of cells of E. coli NIHJ by 70% in 30 minutes in contrast to little or no inhibition of the incorporation of [14C]uridine or [14C]leucine. Under similar conditions, terpentecin did not inhibit either membrane transport (uptake) of [14C]thymidine into the cells or the metabolic conversion of the precursor into various cellular acid-soluble components. Terpentecin at a higher concentration (70 micrograms/ml) inhibited by 40% in 30 minutes the incorporation of [methyl-3H]thymidine triphosphate into the DNA fraction of toluene-treated cells of E. coli JE6296 (pol A-). Terpentecin showed stronger antibacterial activities against Bacillus subtilis M45T (rec-) and E. coli BE1121 (rec A-) than against their corresponding wild type strains. However, terpentecin showed no mutagenicity by the Ames test with Salmonella typhimurium strains TA100, TA98, TA92, TA1538, TA1537 and TA1535, and with E. coli WP2 (uvr A). Terpentecin at a lower concentration (0.07 micrograms/ml) inhibited growth in vitro of mouse leukemia L1210 cells by 50%. With the mammalian cells again the incorporation of [14C]thymidine into the acid-insoluble cell material was inhibited more strongly than incorporation of [14C]uridine and [14C]leucine. There was no sign of mutagenicity by the micronucleus test using mice.

Animals↗
PubMed1985

Isolation and characterization of terpentecin, a new antitumor antibiotic.

A new antitumor antibiotic, terpentecin was isolated from the culture broth of strain MF730-N6. Strain MF730-N6, isolated from soil, was found to belong to the genus Kitasatosporia. The antibiotic was extracted with chloroform, purified by column chromatography using silica gel and Diaion HP-20 successively, and finally purified by high performance reverse-phase thin layer chromatography. The molecular formula of terpentecin was determined to be C20H28O6 (molecular weight, 364). The antibiotic inhibited the growth of Gram-positive and Gram-negative bacteria, and prolonged the survival period of mice bearing leukemia L-1210, P388 and Ehrlich ascites carcinoma.

Actinomycetales↗
PubMed1983

Electrophysiological effects of nicardipine hydrochloride on the isolated sinoatrial and atrioventricular nodes of the rabbit.

The electrophysiological effects of nicardipine-HCl, a new calcium antagonist and potent vasodilator, were studied in the isolated sinoatrial (SA) and atrio-ventricular (AV) nodes of the rabbit in an oxygenated Tyrode solution at 35 degrees C using an intracellular microelectrode technique. Nicardipine-HCl decreased the spontaneous rate of the SA node and prolonged sinus recovery time, dose-dependently. The effective refractory period (ERP) and functional refractory period (FRP) of the AV node and AV conduction time (A-H interval) were also prolonged by nicardipine-HCl in a dose-dependent manner. In conclusion, nicardipine-HCl has electrophysiological effects on the SA and the AV node similar to those of other calcium antagonists in the excised and superfused rabbit heart.

Animals↗
PubMed1982

Electrophysiological effects of disopyramide on hypoxic rabbit ventricular muscle.

Intracellular microelectrode recording techniques were used to elucidate the mechanism of the antiarrhythmic action of disopyramide in an isolated rabbit ventricular muscle perfused by hypoxic Tyrode's solution. Hypoxia induced no significant changes of the resting membrane potential or action potential amplitude but decreased the maximum upstroke velocity of the action potential (dV/dt max) and shortened the action potential duration and the effective refractory period. Disopyramide in a dose of 5 microgram/ml induced a significant decrease of resting membrane potential and action potential amplitude of hypoxic muscle while it did not alter these parameters in oxygenated muscle. Disopyramide depressed dV/dt max in hypoxic muscle as well as in oxygenated muscle. However, there was much greater depression in hypoxic cells. After disopyramide, action potential duration at the 90% level of repolarization and the effective refractory period were prolonged in both hypoxic and oxygenated ventricular muscle. However, disopyramide lengthened the effective refractory period of hypoxic muscle to a much greater degree than that of oxygenated muscle. This resulted in a decrease of disparity in refractoriness. The above differential effects of disopyramide in oxygenated and hypoxic tissue may account for its effectiveness in postinfarction re-entrant arrhythmias.

Action Potentials↗
PubMed1982

An inhibitor of (Na+, K+)-ATPase produced by Streptomyces pseudovenezuelae MF722-02; purification and properties.

A culture product of Streptomyces pseudovenezuelae MF722-02, with a molecular formula of C29H32N2O7, was isolated as yellow needles from culture broths and mycelia of the organism by means of a series of solvent extraction, column chromatography and crystallization. The antibiotic is active against some Gram-positive bacteria, inhibits growth in vitro of cells of mouse leukemia L-1210, prolongs the life span of mice inoculated with the leukemia cells, enhances deoxycholate-induced hemolysis in vitro and inhibits (Na+, K+)-ATPase in vitro.

Animals↗
PubMed1981

Combined effect of verapamil and disopyramide on induction of circus movement tachycardia in patients with pre-excitation.

By means of intracardiac recordings and programmed electrical stimulation of the heart, the combination effect of verapamil and disopyramide on induction of circus movement tachycardia was studied in 8 patients with anomalous extranodal atrioventricular (A-V) pathway. In 4 of 6 patients who manifested reproducible circus movement tachycardia, verapamil, 0.2 mg/kg intravenously administered, prevented the induction of tachycardia by increasing the A-V nodal refractoriness. Disopyramide in a dose of 2 mg/kg was injected 30 minutes after the start of verapamil administration, when prolongation of the A-V nodal conduction time (A-H interval) had continued in most of the patients. Disopyramide lengthened the effective refractory period of the anomalous pathway in all patients in whom this could be determined. The A-H interval, which had been prolonged by verapamil, was shortened in 4 patients and about unchanged in the remaining 4. After addition of disopyramide, sustained tachycardia could be induced in 2 patients who had lost the ability of initiating circus movement tachycardia after verapamil administration. Thus, disopyramide, when administered together with verapamil, may block the effect of verapamil on the A-V node by its anticholinergic action. A concomitant prescription of disopyramide with verapamil in expectation of the depression of both the anomalous pathway and the A-V node may have an untoward outcome.

Adolescent↗
PubMedDate not supplied

Effects of perhexiline maleate on the refractory periods of isolated atrial muscle and atrioventricular node of the rabbit.

The electrophysiologic effects of perhexiline maleate were studied with glass microelectrodes in three types of isolated rabbit heart preparations: (a) sinoatrial node preparation; (b) left atrial free-wall preparation; and (c) atrioventricular node preparation. The spontaneous firing rate of the sinoatrial node was decreased by 10-15% at a concentration of 10(-5) g/ml. The sinus node recovery time after atrial overdrive was prolonged by about 50%. The effective refractory period of the left atrial free wall showed concentration-dependent prolongation at concentrations above 10(-7) g/ml. Although this period was shortened after washing with perhexiline-free Tyrode solution, it did not return to the control lever. The effective refractory period of the right atrium was prolonged by 15% at a concentration of 10(-5) g/ml, but the functional refractory period did not change. The conduction time, effective refractory period, and functional refractory period of the atrioventricular node were significantly increased. Previous reports had claimed that perhexiline had pharmacologic effects on Purkinje fibers and ventricular myocardium at lower concentrations than on the atrium, but we found significant actions on the atrium and the atrioventricular node in therapeutic concentrations.

Animals↗
PubMedDate not supplied

Electrophysiological effects of amiodarone on isolated rabbit heart muscles.

We studied the electrophysiological effects of amiodarone on isolated rabbit heart muscles by conventional microelectrode techniques. It significantly suppressed not only sinus node functions (basic cycle length, sinus recovery time, and corrected sinus recovery time) but also atrioventricular node functions (AH interval, effective refractory period, and functional refractory period) by both superfusion (10 micrograms/ml amiodarone in Tyrode solution) and long-term oral administration (50 mg/day for 2 weeks, then 25 mg/day for 4-6 weeks). On the other hand, oral administration significantly lengthened the action potential duration and effective refractory period of the left atrium and the right ventricle, while superfusion did not. The maximum rate of depolarization, action potential amplitude, and diastolic resting potential were not changed by either route of administration. It is thought that the action of amiodarone on the sinus node and on the atrioventricular node is mainly due to its noncompetitive sympathetic inhibition, and that its action on the left atrium and on the right ventricle is mainly due to reduction of serum triiodothyronine, which requires long-term administration of amiodarone.

Action Potentials↗