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Biomedical subjects

T Tsukada

Publications and source records attributed to T Tsukada.

At least 325 records · Page 18Linked to original sources
PubMed1979

Effects of niludipine (Bay a 7168) on the cardiovascular system with a note on its calcium-antagonistic effects.

1,4-Dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylic acid-bis-(2-propoxyethyl)-ester (niludipine, Bay a 7168), a newly synthesized vasodilator, was three to ten times more potent than nifedipine in dilating the coronary artery of the canine heart-lung and isolated fibrillating heart preparations, but had weaker direct cardiac depressant effects. This drug had a strong and highly selective calcium antagonistic effect on the smooth muscle and also had stronger vasodilating activity on renal and femoral vascular beds as compared to nifedipine. It inhibited myocardial oxidative metabolism in canine and guinea pig hearts.

Animals↗
PubMed1978

Inosine nucleosidase from Azotobacter vinelandii. Purification and properties.

An enzyme catalyzing the hydrolysis of purine nucleosides was found to occur in the extract of Azotobacter vinelandii, strain O, and was highly purified by ammonium sulfate fractionation, DEAE-cellulose chromatography, hydroxylapatite chromatography and gel filtration on Sephadex G-150. A strict substrate specificity of the purified enzyme was shown with respect to the base components. The enzyme specifically attacked the nucleosides without amino groups in the purine moiety: inosine gave the maximum rate of hydrolysis and xanthosine was hydrolyzed to a lesser extent. The pH optimum of inosine hydrolysis was observed from pH 7 to 9, while xanthosine was hydrolyzed maximally at pH 7. The Km values of the enzyme for inosine were 0.65 and 0.85 mM at pH 7.1 and 9.0, respectively, and the value for xanthosine was 1.2 mM at pH 7.1. Several nucleotides inhibited the enzyme: the phosphate portions of the nucleotides were suggested to be responsible for the inhibition by nucleotides. Although the inhibition of the enzyme by nucleotides was apparently non-competitive type with respect to inosine, allosteric (cooperative) binding of the substrate was suggested in the presence of the inhibitor. The physiological significance of the enzyme was discussed in connection with the degradation and salvage pathways of purine nucleotides.

Azotobacter↗
PubMed1978

Chronic lymphocytic leukemia showing pituitary tumor with massive leukemic cell infiltration, and special reference to clinicopathological findings of CLL.

An autopsy case of a 33 years old doctor with chronic lymphocytic leukemia (CLL) was reported. Two remissions were noted with chemotherapy and irradiation. The special characteristic of this case was the tumor formation in the sellar fossa similating a pituitary tumor which was considered as a type of meningeal leukemia, showing visual disturbance. Leukemic cell infiltration was hardly observed in any other organs. From the analysis of five cases of CLL, the author proposes that CLL may be classified into two types: the one is the severe type showing a short clinical course and the other is a mild one, showing a long clinical course. Details such as histopathological findings, cause of death and clinical findings were discussed.

Adult↗
PubMed1978

[Alpha- and beta-adrenoceptor blocking actions of labetalol and effects on the myocardial function, coronary circulation and myocardial energy metabolism thereof (author's transl)].

In the isolated atria, trachea and aorta of the guinea pig and in the heart-lung preparation (HLP) of the dog, labetalol was 3.6 approximately 5.9 times less potent than phentolamine in blocking alpha-adrenoceptors, 1.4 approximately 3.6 times less potent as beta 1-blocker and 6 times less potent as beta 2-blocker than propranolol. Beta 1 and beta 2-blocking actions were 12 approximately 28 and 7 times more potent than alpha-blocking action, respectively. As regards beta 1-blockade, attenuation of the heart rate increase was more prominent than that of the augmentation of the contractile force. Both in the isolated atrial preparation of the guinea pig and in canine HLP, labetalol produced a positive inotropic and chronotropic effect and a slight increase in the coronary flow associated with a slight increase in the myocardial O2 consumption and improvement of the myocardial redox potential. Myocardial extraction and usage of lactate, pyruvate and glucose tended to be decreased and those of FFA decreased significantly. The positive inotropic and chrontropic effect was observed in HLP of 6-hydroxydopamine-pretreated dogs and was abolished with propranolol. Labetalol produced a relaxation of the isolated trachea of the guinea pig, which was inhibited with propranolol. In doses higher than those required for alpha- and beta-adrenoceptor blockade, labetalol produced calcium-antagonistic action.

Adrenergic alpha-Antagonists↗
PubMed1978

Antiarrhythmic effect of oxprenolol on halothane-epinephrine and coronary ligation induced ventricular arrhythmias in beagle dogs.

Antiarrhythmic effects of oxprenolol, a beta-blocker, were studied quantitatively on arhythmias produced by epinephrine during halothane anesthesia and by two-stage coronary ligation, and were compared to those of other beta-blockers, propranolol and Kö 1400, which have been already reported. Though oxprenolol has potent beta-blocking activity, the antiarrhythmic effect on halothane-epinephrine arrhythmia was significantly weaker than those of propranolol and Kö 1400. The effective dose of oxprenolol was 60 +/- 18 microgram/kg (mean +/- S.E., N = 6), which is in the range of the so-called beta-adrenergic blocking dose. The weaker antiarrhythmic effect of oxprenolol as compared to propranolol and Kö 1400 is probably due to the intrinsic positive chronotropic effect, which is most clearly observed in oxprenolol as compared to the other two drugs. As for two-stage coronary ligation arrhythmia, oxprenolol suppressed only that observed 48 hours after coronary ligation using higher doses (5 to 10 mg/kg). Other beta-blockers also showed similar effects. Because of the high doses necessary for the antiarrhythmic effects on the coronary ligation arrhythmia, the mechanism for suppressing the arrhythmia is probably due to the local anesthetic action of the beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1978

Hypotensive and vascular effects of labetalol in the normotensive rat and dog.

A new antihypertensive agent, labetalol, has potent hypotensive effects in the anesthetized rat and dog when given intravenously and also in the unanesthetized beagle when given orally. Labetalol slightly increased renal blood flow of the anesthetized dog while decreasing blood pressure. Labetalol slightly increased blood flow of canine femoral artery under constant pressure perfusion. However as compared with hydralazine, labetalol seems to have no marked vasodilatatory effect which accounts for its hypotensive effect. Pharmacologically, labetalol possessed both alpha- and beta-blocking activities, though weaker than phentolamine and propranolol respectively. Another specific action of labetalol was that it has stronger beta-blocking action on beta1 receptor (heart rate response) than on beta2 receptor (blood pressure response). Like several other beta-blockers, labetalol seems to block neuronal uptake of noradrenaline.

Adrenergic alpha-Antagonists↗
PubMed1978

Effects of heart rate and isoproterenol on the functional refractory period of the AV node.

The effects of heart rate and l-isoproterenol on the functional refractory period (FRP) of the atrioventricular (AV) node were analyzed in anesthetized dog. A rectangular hyperbola was adopted to express the relationship between the AV conduction time of the premature beats and the atrial coupling intervals. FRP was shown to be expressed as FRP = E + 2 square root of C - C/(T - E). Thus, it is a function of the effective refractory period (E), basic cycle length (T), and C, a constant. A decrease in the basic cycle length caused a decrease in the effective refractory period as well as FRP; the minimum conduction time remained unchanged. As expected from the above equation, relationship of FRP to the basic cycle length was curvilinear. The above equation also indicates that changes in FRP produced by a change in the basic cycle length were to be ascribed to the change in the AV conduction time of the basic beats. Therefore, FRP under this condition cannot be equated with the refractory period in its true sense. In the paced hearts, l-isoproterenol hydrochloride caused a decrease in the effective refractory period, FRP, C and the minimum conduction time, and the changes in FRP were shown to be correlated with the changes in the effective refractory period, indicating that the change in FRP attained in a given fixed cycle length may be due to a change in the effective refractory period.

Animals↗