Method for the fluorimetric estimation of dopamine.
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Biomedical subjects
Publications and source records attributed to T Seki.
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Effects of ergocornine and reserpine on tail resorption during metamorphosis in Bufo bufo japonicus tadpoles were studied. At prometamorphosis, ergocornine induced precocious tail resorption, while reserpine scarcely affected the tail size. At the climax of metamorphosis, ergocornine was almost ineffective in accelerating tail resorption, while reserpine was effective in inhibiting tail resorption. Since prolactin-like hormone is known to block the tail resorption induced by thyroid hormones, it was postulated that the release of the hormone is blocked by ergocornine during prometamorphosis and stimulated by reserpine during climax.
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This study was undertaken to investigate influences of a new vasodilator, YC-93, a derivative of 1,4-dihydropyridine, on cerebral circulation and cerebrovascular CO2 reactivity. Cerebrocortical PO2, cerebrocortical PCO2, cerebrocortical blood flow and arterial blood pressure were continuously recorded by means of a PO2 electrode, a PCO2 electrode and a plate-type crossed thermocouple flowmeter placed on an exposed pial surface of the cat brain. The changes in each parameter induced by YC-93 were compared with those induced by papaverine hydrochloride. The effects of 5% CO2 inhalation were compared before and after the intravenous injection of YC-93. YC-93 (0.01 mg/kg) showed a more marked and longer-lasting hypotensive effect that papaverine (1 mg/kg) and yet produced a significant increase in cerebrocortical PO2. After the administration of YC-93, the degree of the increase in cerebrocortical PO2 during 5% CO2 inhalation was reduced significantly in comparison with that before the administration. The above data indicates that YC-93 has a vasodilating effect on cerebral blood vessels and that the drug causes a decrease in cerebrovascular CO2 reactivity.
1 In order to determine the optimal level of electrical stimulation, the degree of pain sensitivity produced by electrical stimulation on the volar side of terminal phalange of the right forefinger was studied in 22 male and female volunteers between the ages of 20 and 27 years. 2 A stimulation frequency of 400 Hz, width of 0.1 ms and electrical potential of 55 V was found to be optimal for study fo analgesics. 3 The effect of acetylsalicylic acid was studied in 40 healthy male volunteers between the ages of 20 and 25 years. Electrical stimulation was applied for 5 s under a single-blind method at a frequency of 400 Hz, width of 0.1 ms and electrical potential of 25, 35 and 55 V. Placebo, 250 mg, 500 mg and 1 000 mg of acetylsalicyclic acid were administered orally under double-blind method conditions. 4 As a result of this study, it was found that acetslsalicylic acid in a dose of 500 and 1 000 mg, was effective in relieving pain with statistically significant differences from a placebo.
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The effect of indapamide, a high ceiling diuretic, antihypertensive drug, was investigated in helically-cut strips of rabbit cerebral, coronary, renal, mesenteric and femoral arteries and aortae. The addition of indapamide in concentrations higher than 3 X 10(-5)M relaxed those arterial strips contracted with prostaglandin F2alpha; the relaxation being greater in cerebral, coronary and renal arteries. Atropine propranolol and aminophylline did not reduce the relaxing effect. Hydrochlorothiazide produced fewer incidences of relaxation. Treatment for 20 min with indapamide (3 X 10(-5) or higher) significantly attenuated the contractile response of mesentric arteries to nicotine and tyramine. Contractile responses to transmural electrical stimulation were not reduced but rather potentiated. The dose-response curve of norepinephrine was not significantly affected by indapamide. The contractile response of nictitating membranes of anesthetized cats to stimulation of preganglionic sympathetic nerves was not influenced by indapamide but was abolished by hexamethonium. It may be concluded that arterial relaxations induced by indapamide are due to a direct action on smooth muscles. Indapamide appears to attenuate the response to nicotine and tyramine by interfering with the mechanism of neuronal amine uptake. However, such does not involve a ganglionic blockade nor a reduction of the release of norepinephrine from adrenergic nerve terminals.
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