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Biomedical subjects

T Kitani

Publications and source records attributed to T Kitani.

At least 253 records · Page 14Linked to original sources
PubMed1981

[Therapeutic effect of ticarcillin against severe infection in patients with hematologic malignancy (author's transl)].

Seventy patients with severe infection accompanying hematologic disorders including leukemia and lymphoma were treated with ticarcillin in combination with aminoglycosides and/or cephem derivatives. Of the 58 patients in whom the efficacy could be evaluated, 17 (29%) responded markedly and 22 (38%) moderately, the effective rate being 67%. Side effects attributable to the treatment were noted: rash in 2, fever and rash in 1, vascular pain in 2 (5 and 7 years of age). Renal and hepatic functions were abnormal in 4 each. However, these abnormal findings were not attributed to ticarcillin. These results indicate that ticarcillin is an effective and safe antibiotic for the treatment of severe infection accompanying hematologic malignancy when used in combination with aminoglycosides and/or cephem derivatives.

Adult↗
PubMed1980

Effect of trapidil on prostacyclin generation of arterial wall.

Prostacyclin (PGI2) has been reported to be a labile but potent inhibitor of platelet aggregation and a powerful vasodilator. This paper reports the effect of trapidil on PGI2 generation in rat aorta by means of bioassay system. The aortic ring was incubated in 0.05 M Tris HCl buffer (pH 7.5) for 10 min. This incubation medium was added into human PRP, and then incubated at 37 degrees C for 2 min., and ADP was added. PGI2 activity was assayed by the inhibitory percentage of ADP induced platelet aggregation. When the aortic ring was incubated in a medium containing trapidil, PGI2 generation was accelerated. This acceleration was inhibited by pretreatment with indomethacin. Moreover, the aortas of rats intravenously injected with 30 mg/kg of trapidil were incubated in the same way, and PGI2 activity in the medium was estimated. More potent PGI2 activity was observed in the aortas of rat treated with trapidil compared with the controls. These results indicate that acceleration of PGI2 generation from aorta by trapidil is involved in the mode of action of this drug of thrombus formation.

Animals↗
PubMed1980

Thrombocytopenia in Graves' disease: effect of T3 on platelet kinetics.

A study was carried out in which the platelet count was decreased in approximately half the patients with hyperthyroidism and gradually increased with treatment. Platelet disappearance curves were curvilinear and the platelet survival was shortened in the hyperthyroid state. Patients maintained in a euthyroid state for 3 months or less continued to have a shortened platelet survival. The survival returned to normal after 6 months or more of euthyroid status. In order to clarify the cause of the decreased platelet count in the patients, animal experiments were performed. T3-injected rats had decreased platelet counts and shortened platelet survival. When platelets obtained from T3-injected rats were transfused to a control group of untreated rats, the platelet survivals were normal. When platelets obtained from the control group of rats were transfused to T3-injected rats, the platelet survivals were shortened. Disappearance of heat-damaged RBC from the circulation was also accelerated in T3-injected rats. This suggests that thrombocytopenia in Graves' disease is caused by an increased sequestration potency of the reticuloendothelial phagocyte system stimulated by thyroid hormone.

Animals↗
PubMed1980

Effect of sodium loading and depletion on vascular reactivity and prostacyclin generation.

In order to estimate the modulatory activity of Prostacyclin (PGI2) to the vascular reactivity, pressor responses to angiotensin II (A II) and noradrenaline (NA) and PGI2 generation aorta were measured using the rats of sodium loading or of sodium depletion. On the sodium loading, the blood pressure increased gradually and plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were decreased. The pressor responses to A II and NA were enhanced by sodium loading. The PGI2 generation of aorta was enhanced at the initial stage of sodium loading and decreased thereafter. The increased generation of PGI2 may represent the adaptive mechanism for the attenuation of the sustained elevation in blood pressure. It sodium depletion, the pressor responses to A II and NA were decreased, and PRA and PAC were elevated. PGI2 generation of aorta was also increased. These findings suggested that PGI2 could participate in blood pressure control mechanism on sodium loading and depletion.

Aldosterone↗
PubMed1980

Hereditary and acquired abnormalities in erythrocyte phosphofructokinase activity: the close association with altered 2,3-diphosphoglycerate levels.

Specific deficiency of erythrocyte phosphofructokinase (PFK) activity in Type VII glycogenosis presents a good model for the analysis of the relationship between 2,3 diphosphoglycerate (2,3 DPG) level and glycolysis in erythrocytes since glycolytic flow is partially blocked at the regulatory step. Enzymatic analyses of glycolytic intermediates of erythrocytes from a patient with Type VII glycogenosis demonstrated that 2,3 DPG is markedly decreased in parallel with fructose-1,6-phosphate (FDP). In acidosis including diabetic ketoacidosis and uremic acidosis a fall in 2,3 DPG is also associated with a marked reduction in FDP. On the other hand, in respiratory alkalosis glycolytic intermediates shift to the opposite direction and forward crossover at PFK step appears, being associated with an elevation of 2,3 DPG. These data indicate a close relationship between 2,3 DPG level and PFK activity in erythrocytes. At least in acidosis and alkalosis the alteration in 2,3 DPG level may well be explained by changes in PFK activity caused mainly through allosteric mechanism. In addition, twelve cases with hereditary PFK deficiency in muscle and erythrocytes reported in the world are reviewed and discussed briefly.

Alkalosis↗
PubMed1979

[Thrombokinetics].

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Blood Cell Count↗