Biomedical subjects

E Osada

Publications and source records attributed to E Osada.

16 recordsLinked to original sources

PubMed1996

Prosthodontic treatment for a patient with advanced hydantoin-associated gingival hyperplasia: a case report.

A patient in whom gingival hyperplasia was caused by prolonged use of an anticonvulsant drug (hydantoin) is described. Advanced gingival hyperplasia and significant displacement of the remaining teeth caused severe damage, especially to the patient's appearance. It was not possible to cure the problems completely with routine periodontal treatment. It was decided to extract all the remaining teeth and restore function and esthetics early with complete dentures. Cephalometric analysis was used to determine the degree to which the teeth had drifted. During fabrication of the dentures, the analysis was very useful in deciding the position of the anterior teeth and checking the vertical dimension of occlusion.

Adult↗

PubMed1993

[Study on platelet satellitism].

The platelet leukocyte adherence phenomenon, so-called 'Platelet Satellitism (PS)', was recognized on peripheral blood smear from ethylenediaminetetraacetic acid (EDTA)-anticoagulated blood in two patients. The present study was undertaken to elucidate both inducing and inhibitory factors for PS by utilizing two patients' blood. Both heparin and sodium citrate could not induce PS in these patients. This phenomenon was inhibited by anti-platelet membrane glycoprotein (GP) IIb/IIIa complex antibody (AP-2), but not by antibodies against platelet membrane glycoprotein (GP) Ib/IX complex, fibrinogen and von Willeb and factor. Patients' sera were subjected to column chromatography of Sephacryl S-300 to obtain immunoglobulin (Ig) G, IgA and IgM fractions. In one patient, IgG fraction, but neither IgA nor IgM fractions could induce PS phenomenon in normal whole blood, while IgA but neither IgG nor IgM could induce PS in another patient. Furthermore, when purified IgG from the first patient was treated with 2U/ml of plasmin to digest Fc portion, PS phenomenon disappeared. The F(ab')2 portion was prepared from whole IgG treated with pepsin, then added to normal whole blood. Purified F(ab')2 fragment by itself could not induce PS phenomenon, whereas the preincubation of F(ab')2 in normal whole blood could inhibit the PS caused by the patient's whole IgG. These results indicate that platelet membrane glycoprotein (GP) IIb/IIIa complex and both Fab and Fc portions of immunoglobulin might be necessary to induce PS phenomenon in EDTA-anticoagulated whole blood.

Adult↗

PubMed1987

Antithrombotic effect of TRK-100, a novel, stable PGI2 analogue.

TRK-100, a stable PGI2 analogue structurally different from carbacyclines, was compared with other antiplatelet drugs for its effect on platelet functions using animal models. TRK-100 (10-300 nM) inhibited rat platelet aggregation induced by ADP (3 microM), collagen (12.5 micrograms/ml) and A23187 (10 microM), and its potency was about 1/3-1/7 that of PGI2. TRK-100 (0.3-3 mg/kg, p.o.) dose-dependently inhibited rabbit platelet adhesion (ED50: 2.2 mg/kg), and its effect lasted over at least 5 hr. In contrast, aspirin and ticlopidine (both at 300 mg/kg, p.o.) showed only a slight inhibition (4-7%). In the thrombocytopenia induced by collagen injection in rats, TRK-100 (3-300 micrograms/kg, i.v.; 0.1-3 mg/kg, p.o.) dose-dependently inhibited a decrease in platelet number, and its ED50 was 0.48-0.62 mg/kg orally and 13.7-16.4 micrograms/kg intravenously, while the inhibition by aspirin and ticlopidine (both at 1000 mg/kg, p.o.) was 40 and 37%, respectively. In the experimental thread thrombosis in rats. TRK-100 (0.03-3 mg/kg, p.o.) dose-dependently inhibited thrombus formation, and its ED50 was 0.46 mg/kg, being 21 and 87 times as potent as aspirin and ticlopidine, respectively. These results reveal that TRK-100 has a potent antiplatelet activity and is orally and intravenously effective for a variety of thrombosis models, suggesting that it may have a therapeutic value as an antithrombotic drug.

Animals↗

PubMed1984

Pharmacological studies of mabuterol, a new selective beta 2-stimulant. I: Bronchodilating effect.

The bronchodilating effect and other related pharmacological properties of dl-1-(4-amino-3-chloro-5-trifluoromethyl-phenyl)-2-tert.-butylamino-etha nol hydrochloride (mabuterol) were studied in comparison with those of isoprenaline (isoproterenol), salbutamol and procaterol. In relaxing the isolated normal tracheal muscle in guinea pigs, mabuterol was more potent than isoprenaline and salbutamol, and the effect seemed to be due to the activation of beta-adrenoceptors because it was inhibited by propranolol. In anesthetized guinea pigs, mabuterol given i.v. was less potent but showed a longer duration of action than isoprenaline and salbutamol in inhibiting an increase in the bronchial resistance induced by acetylcholine, histamine and serotonin. When given intraduodenally, it was 1.9-7.8 times more potent than isoprenaline and salbutamol. In conscious guinea pigs, mabuterol given subcutaneously was less potent than isoprenaline and salbutamol in experimental asthma induced by acetylcholine, histamine and antigen, but 26-102 times more potent than the reference bronchodilators when given orally. Chronic oral treatment of mabuterol showed no significant change in the inhibitory effect on the experimental asthma and no development of tolerance was observed. In the maximum increase in the heart rate in conscious guinea pigs, mabuterol given orally was less potent than isoprenaline and salbutamol. Calculation of the selectivity ratio of the drugs for the bronchial muscle vs. cardiac muscle indicated that mabuterol was about 7.4 times more selective for the bronchial muscle than salbutamol.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1984

Pharmacological studies of mabuterol, a new selective beta 2-stimulant. II: Effects on the cardiovascular system and smooth muscle organs.

Effects of dl-1-(4-amino-3-chloro-5-trifluorome-thyl-phenyl)-2-tert.-bu tylamino-ethanol hydrochloride (mabuterol) on the cardiovascular system and smooth muscle organs were investigated in comparison with those of isoprenaline (isoproterenol), salbutamol and procaterol, and the following results were obtained. Mabuterol (i.v.) produced a dose-dependent decrease in the blood pressure at doses ranging from 0.3-1000 micrograms/kg, and the heart rate was slightly increased at 0.3-30 micrograms/kg but decreased at 100-1000 micrograms/kg in rats, cats and dogs. The effects of mabuterol on the blood pressure, total peripheral vascular resistance (TPR) and heart rate were respectively 14, 37 and 104 times less potent than those of isoprenaline and there were none on the maximum dp/dt in the left ventricle in cats. In dogs, mabuterol had 356 and 118 times less effect on the blood pressure and TPR than isoprenaline and slightly increased the heart rate and maximum dp/dt. Mabuterol (p.o.) decreased the blood pressure at doses ranging from 3 micrograms-100 mg/kg, and the heart rate was increased at 3 micrograms-10 mg/kg, but decreased at 100 mg/kg in conscious and anesthetized rats. In the guinea pig atria, mabuterol slightly increased the heart rate and contractile force, but in the electrically driven left atrium mabuterol had no effect whereas procaterol slightly increased the contractile force. Mabuterol inhibited the positive inotropic effect of isoprenaline at 10(-7) g/ml and decreased the maximum driving frequency at 3 X 10(-6) g/ml. Mabuterol was 3 times more potent in relaxing the isolated rat uterus, but 700 times less potent than isoprenaline in relaxing the rabbit jejunum. Mabuterol (p.o.) depressed the intestinal propulsion and was equipotent to isoprenaline and 2.5 times less potent than salbutamol. Mabuterol had no effect on alpha-adrenergic, acetylcholine and histamine receptors. These results suggest that mabuterol has a specific effect on beta 2-adrenoceptors with no beta 1-stimulation. In addition, mabuterol exhibited beta 1-blocking activity at dosages 200-300 times higher.

Adrenergic beta-Agonists↗

PubMed1984

Pharmacological studies of mabuterol, a new selective beta 2-stimulant. III: Effects on the central nervous system, striated muscle and carbohydrate and lipid metabolism.

Effects of dl-1-(4-amino-3-chloro-5-trifluoromethyl-phenyl)-2-tert.-butylamino-etha nol hydrochloride (mabuterol) on the central nervous system, the striated muscle and the carbohydrate and lipid metabolism were investigated in comparison with those of isoprenaline and salbutamol. Mabuterol caused the following changes in behavior: increased touch response (10 mg/kg p.o.), decreased spontaneous movement and ptosis (30 and 100 mg/kg p.o., resp.), observed for 240-300 min. Mabuterol (5 mg/kg p.o. and 2.5 mg/kg s.c.) prolonged the sleeping time induced by hexobarbital Na, but not dose-dependently. Mabuterol depressed reactive movement at 80 mg/kg p.o. and 40 mg/kg s.c. in the rotarod test, at 160 mg/kg p.o. and 40 mg/kg s.c. in the traction test and at 200 mg/kg p.o. and 160 mg/kg s.c. in the inclined plane test in mice, whereas isoprenaline and salbutamol were almost ineffective. Analgesic activity of mabuterol was found in the acetic acid writhing test but not in the bradykinin-induced nociception test. An anticonvulsive effect was not observed. Mabuterol (10 mg/kg i.v.) produced a change in the spontaneous EEG of one of three rabbits, showing synchronization of cortical activity with sedation. Equipotent dose (i.v.) ratios of mabuterol to isoprenaline were 10.2, 30 and 133 in the depression of incomplete tetanic contraction of cat soleus muscle, hypotensive effect and tachycardia respectively, whereas neither indirect nor direct electrical stimulation induced contraction of diaphragm and gastrocnemius muscle was affected. Equipotent dose (s.c.) ratios of mabuterol to isoprenaline were 2.07, 4.64 and 3.21 in increasing plasma levels of glucose, lactic acid and free fatty acids respectively. Mabuterol caused no remarkable change in myocardial glycogen content.

Adrenergic beta-Agonists↗

PubMed1984

Pharmacokinetic studies of mabuterol, a new selective beta 2-stimulant. II: Urinary metabolites of mabuterol in rats and their pharmacological effects.

A selective beta 2-stimulating bronchodilator, dl-1- (4-amino-3-chloro-5-trifluoromethyl-phenyl)-2-tert.-butyl-amino-ethanol hydrochloride (mabuterol), is mainly metabolized by oxidative deamination pathway. Unchanged mabuterol and the following 6 types of metabolites, M-1 (hydroxylation of tert.-butyl group), M-2 (glycol), M-3 (mandelic acid), M-4 (aldehyde), M-5 (benzoic acid) and M-6 (hippuric acid) were identified by thin-layer chromatography and mass spectroscopy. Pharmacologically, only M-1 had effects on the airway resistance, blood pressure and heart rate, and the isolated organs. But its selective beta 2-stimulating effect was 2-10 times lower than that of mabuterol. M-1 antagonized the positive inotropic action induced by isoprenaline (isoproterenol). Other metabolites showed no appreciable activity.

Adrenergic beta-Agonists↗

PubMed1980