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Biomedical subjects

K Takeda

Publications and source records attributed to K Takeda.

At least 1,351 records · Page 75Linked to original sources
PubMed1980

Peripheral effects of guanfacine compared to those of clonidine in the dog.

Comparative studies of the antihypertensive agents, guanfacine and clonidine, on their peripheral effects were performed using normotensive canine preparations. On the peripheral vascular beds, both drugs constricted cerebral renal and femoral vasculatures, but there were no decreases in the renal blood flow. This vasoconstriction was blocked by phentolamine, and guanfacine was about 3 times less potent than clonidine. Both drugs contracted the canine nictitating membrane, and had no effect on the ganglionic transmission in the cervical sympathetic ganglion. Qualitatively different effects were observed in their effects on renal function. Guanfacine slightly increased the urinary volume and Na excretion, while clonidine increased the urinary volume and K excretion. All these peripheral effects do not seem to be responsible for their hypotensive effect.

Animals↗
PubMed1980

Effects of piridoxilate, a glyoxylic acid derivative, on the energy metabolism of the heart.

Piridoxilate is a conjugation product of pyridoxine and glyoxylic acid, which may be a physiological regulator of cell respiration. Effects of this substance on the oxidation-reduction state of the pyridine nucleotides in the heart were studied using the canine heart-lung preparation supported by a donor dog. The oxidation-reduction state of the heart was estimated using the following 2 parameters: 1) myocardial redox potential and 2) NADH fluorescence in the heart muscle. In doses above 0.4 mM, piridoxilate produced a marked shift to more positive values of the myocardial redox potential and a decrease in NADH fluorescence. In contrast, ventilation of the animal with N2 gas and infusion of NaCN into the preparation resulted in a shift to more negative values of myocardial redox potential and an increase in NADH fluoresecence of the heart muscle. After pretreatment of the preparation with piridoxilate, the depression of redox potential and the increase in NADH fluorescence produced by N2 gas inhalation or by NaCN infusion were clearly reduced. These findings suggest a protective action of piridoxilate against hypoxia which may be attributable to rearrangement of the myocardial metabolism.

Animals↗
PubMed1980

[Intravenous chronic toxicity of lentinan in rats: 6-month treatment and 3-month recovery (author's transl)].

Chronic toxicity of lentinan was studied in male and female JCL : SD rats. Lentinan was given intravenously into tail vein. Dosage levels employed were 0 (5% mannitol), 0.01, 0.1, 1 (with or without dextran), and 10 mg/kg/day for 6 months in a volume of 1 ml/100 g body weight. After 6 months, the treatment was discontinued and a recovery study was performed for 3 months. Rats receiving 10 mg/kg had redness and necrosis of the tail, the treatment was stopped at week 5, and the rats were sacrificed. Rats receiving 1 mg/kg showed redness of the ear, tail, and scrotum, which was remarkable in the 2nd and 3rd months. Body weight gains were not adversely affected. Laboratory examinations revealed an increase in leukocyte count, decreases in differential eosinophil count and platelet count, and an increase in serum beta-globulin level in drug-treated rats. At autopsy after 6 months, rats from the drug-treated groups had pulmonary hemorrhage and enlargements of the spleen and mesenteric lymph nodes. Histologic changes attributable to treatment included (1) activation of reticulo-endothelial system such as small epithelioid cell nodule in the liver, spleen, and mesenteric lymph nodes, and mobilization of Kupffer cells; (2) arteritis in various organs, especially notable in the spleen, testis, and epididymis ; (3) hemorrhage in the lung; and (4) hypospermatogenesis. All these changes described above had a propensity to recover. The maximum no effect level was estimated to be less than 0.01 mg/kg in the present study in male and female rats.

Animals↗
PubMed1980

H + -substrate cotransport by the melibiose membrane carrier in Escherichia coli.

Proton entry into anaerobic Escherichia coli in response to the addition of HCl was measured by monitoring pH changes in the external solution. Preincubation of cells in a Na+ -free medium containing melibiose or methyl-alpha-galactoside (alpha MG) stimulated the rate of H+ entry in response to the acid pulse. This melibiose- or alpha MG-dependent proton pathway appeared to be identical to the melibiose carrier, since the channel was only observed in melibiose-induced cells. Furthermore, this membrane pathway for protons showed the same temperature sensitivity as the melibiose carrier (active at 30 degrees but inactive at 37 degrees). These observations are consistent with the idea that the melibiose transport system provides a pathway for protons in the presence of appropriate substrates, but that the pathway is closed to protons in the absence of the sugar. Such observations indicate that there is an obligatory coupling between H+ flux and melibiose or alpha MG flux through the carrier when Na+ is omitted from the incubation medium.

Biological Transport↗
PubMed1979

Retroperitoneal hemangiopericytoma associated with hypoglycemia: report of a case.

A 34-year-old woman had episodes of hypoglycemic attack 8 years after a surgical resection of a retroperitoneal hemangiopericytoma. In spite of normal levels of serum IRI, insulin radioreceptor assay demonstrated high level of plasma ILA (insulin like activity). The patient underwent resection of a recurrent retroperitoneal tumor with metastatic lesions of the liver. Postoperatively, ILA level in plasma by insulin radioreceptor assay decreased, and hypoglycemic attacks disappeared. Therefore, this associated hypoglycemia was presumed to be not caused by excess glucose consumption by the tumor, not by excess secretion of IRI by the tumor, but caused by the presence of high level of ILA related to the tumor.

Adult↗
PubMed1979

Sympathetic hyperresponsiveness to hypothalamic stimulation in young hypertensive rats.

The possible occurrence of central sympathetic dysfunction during development of spontaneous hypertension was studied by recording aortic pressure and sympathetic nerve activity concurrently during electrical stimulation of the posterior hypothalamus in 9-wk-old Kyoto-Wistar rats. Even at this early age, basal levels for both measurements were already elevated significantly in those with spontaneous hypertension. Increases in sympathetic neural firing induced by graded hypothalamic stimulation were always followed by corresponding increases in blood pressure; magnitude of both effects was appreciably larger in spontaneously hypertensive than in normotensive rats, as was the vasodepression caused by blocking autonomic ganglia with pentolinium. By contrast, pressor responses to injected norepinephrine were almost equal thereby suggesting that cardiovascular reactivity was unaltered and that enhanced responsiveness to hypothalamic stimulation was directly due to the concomitant increase in sympathetic nerve activity. Although the exact site from which sympathetic hyperactivity originates was unidentified, our results support the interpretation that sympathetic mechanisms involving the posterior hypothalamus participate in elevating blood pressure during development of spontaneous hypertension in rats.

Animals↗
PubMed1979

Effects of several beta-blocking agents on the development of hypertension in spontaneously hypertensive rats.

Antihypertensive effects of chronic oral administration of adrenergic beta-blocking agents were assessed in SHR. Propranolol, pindolol, oxprenolol, atenolol and labetalol were used as beta-blockers and the effects of these compounds on the blood pressure and the heart rate were compared with those of hydralazine, a representative vasodilating antihypertensive agent. Propranolol, oxprenolol and atenolol produced a definite decrease in the heart rate; the development of hypertension was retarded. Pindolol produced antihypertensive effects only after a longer period of administration and such were associated with insignificant decrease in heart rate. With a shorter period of administration the drug produced only an insignificant fall of blood pressure with practically no change in the heart rate. With labetalol, a beta-blocker with alpha-blocking action, a fall of blood pressure appeared earlier and was of greater magnitude. Hydralazine produced a definite antihypertensive effect, which appeared immediately after administration and was associated with a tachycardia. In pithed rats, only pindolol produced a definite fall of blood pressure. On the basis of these findings, possible mechanisms of antihypertensive effects of beta-blockers were discussed.

Adrenergic beta-Antagonists↗
PubMed1979

Effects of 2-nicotinamidoethyl nitrate on the cardiovascular system.

Using the dog as experimental animal, effects on the cardiovascular system of a new vasodilator, 2-nicotinamidoethyl nitrate (SG-75), were studied. In the heart-lung preparation, the compound produced a dose-dependent increase in the coronary blood flow, which was associated with only a minimal increase in the myocardial oxygen consumption. There was essentially no change in the myocardial function. The myocardial redox potential was shifted to more positive values. In the isolated perfused heart preparation (Langendorff's preparation), SG-75 produced a dilatation of only the small resistive arterioles. However, it produced a dilatation of the large conductive artery in underperfused myocardium. SG-75 produced a significant increase in the cerebral venous outflow, associated with an increase in the cerebro-spinal fluid pressure. It produced a reducation of the venous return, which was especially prominent in the lower half of the body. In the isolated smooth muscle preparation of the coronary artery, high-doses of SG-75 induced calcium antagonistic effects and produced a relaxation of the lanthanum contracture.

Animals↗
PubMed1979

[Chronic toxicity test of 4-ethoxy-2-methyl-5-morpholino-3(2H)-pyridazinone (M73101) in beagle dogs (author's transl)].

Male and female dogs, aged 17--21 months, were administered orall M 73101 (0, 60, 120 and 240 mg/kg/day), a new analgesic and antiinflammatory drug, for 27 weeks, and following recovery test was carried out for 5 weeks. Dead animals were not found throughout the experimental period. Body weight gain, and food and water consumption were not affected due to M 73101 administration. Except for a slight increase of vomitting in the highest dose, there were no abnormal symptoms. Biochemical examination showed the slight increase in serum alkaline phosphatase activity and free cholesterol level. Pathological examination revealed a dose-dependent increase of liver weight and hypertrophy of hepatocytes due to proliferation of smooth endoplasmic reticulum. In addition, mitochondria became irregularly large in the highest dose. There were no abnormal findings in the gastro-intestinal tracts except for an erosion of gastric mucosa, which was noted in a female dog treated 240 mg/kg/day of M 73101. From these results, it was suggested that the maximum non-toxic dose was 60 mg/kg/day or less, and the greatest safety dose was 120 mg/kg/day in beagle dogs.

Animals↗