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Biomedical subjects

T Satake

Publications and source records attributed to T Satake.

At least 37 records · Page 2Linked to original sources
PubMed1991

Quantitative estimation of infarct size by simultaneous dual radionuclide single photon emission computed tomography: comparison with peak serum creatine kinase activity.

To test the hypothesis that simultaneous dual energy single photon emission computed tomography (SPECT) with technetium-99m (99mTc) pyrophosphate and thallium-201 (201TI) can provide an accurate estimate of the size of myocardial infarction and to assess the correlation between infarct size and peak serum creatine kinase activity, 165 patients with acute myocardial infarction underwent SPECT 3.2 +/- 1.3 (SD) days after the onset of acute myocardial infarction. In the present study, the difference in the intensity of 99mTc-pyrophosphate accumulation was assumed to be attributable to difference in the volume of infarcted myocardium, and the infarct volume was corrected by the ratio of the myocardial activity to the osseous activity to quantify the intensity of 99mTc-pyrophosphate accumulation. The correlation of measured infarct volume with peak serum creatine kinase activity was significant (r = 0.60, p less than 0.01). There was also a significant linear correlation between the corrected infarct volume and peak serum creatine kinase activity (r = 0.71, p less than 0.01). Subgroup analysis showed a high correlation between corrected volume and peak creatine kinase activity in patients with anterior infarctions (r = 0.75, p less than 0.01) but a poor correlation in patients with inferior or posterior infarctions (r = 0.50, p less than 0.01). In both the early reperfusion and the no reperfusion groups, a good correlation was found between corrected infarct volume and peak serum creatine kinase activity (r = 0.76 and r = 0.76, respectively; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Enzyme Tests↗
PubMed1991

Prostaglandin H2 as an endothelium-derived contracting factor and its interaction with endothelium-derived nitric oxide.

The possibility that prostaglandin H2 is an endothelium-derived contracting factor (EDCF) was evaluated in rings of thoracic aorta of spontaneously hypertensive rats (SHR). When the aortic rings were contracted with norepinephrine (10(-7) mol/l) and treated with acetylcholine (10(-5) mol/l), a relaxant response with a peak after approximately 1 min and a contractile response with a peak after approximately 7 min were observed. When these rings were pretreated with a thromboxane A2/prostaglandin H2 receptor antagonist (ONO-3708), the later contractile response was clearly inhibited and only a sustained relaxant response was observed. This relaxant response was completely inhibited by pretreatment with an inhibitor of nitric oxide production (N-nitroarginine methylester; NNM). When aortic rings in the basal condition were treated with NNM and then with acetylcholine, a contractile response with a peak after 7 min was observed, but this reaction was completely inhibited by pretreatment with ONO-3708. The rate of 6-keto-prostaglandin F1 alpha production showed a peak of 1.4 x 10(-6) mol/l per min per tissue, 2-4 min after administration of acetylcholine. With exogenous prostaglandin H2 (5 x 10(-7) mol/l), a peak contraction was observed after approximately 4 min, the degree and pattern of which were similar to that induced by acetylcholine. Endogenous prostaglandin H2 is considered to be produced by the aortic rings in an amount sufficient to induce vascular contraction within 30 s, and the pattern of this contraction induced by acetylcholine resembles that induced by exogenous prostaglandin H2. These findings most strongly suggest that prostaglandin H2 is an EDCF.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Inhibition of cyclic GMP phosphodiesterase by xanthine derivatives relaxes guinea-pig trachealis smooth muscle.

1. For the purpose of clarifying the mechanism of the airways smooth muscle relaxant action of xanthines, cyclic guanosine monophosphate (GMP) phosphodiesterase (PDE) from guinea-pig trachealis muscle was purified with diethylaminoethyl ether (DEAE) cellulose column chromatography. 2. Five 3-alkylxanthines (3-methylxanthine, 3-ethylxanthine, 3-n-propylxanthine (enprofylline), 3-n-butylxanthine, and 3-iso-butylxanthine), and five 1-methyl-3-alkylxanthines (1-methyl-3-methyl-xanthine (theophylline), 1-methyl-3-ethylxanthine, 1-methyl-3-n-propylxanthine, 1-methyl-3-n-butylxanthine, and 1-methyl-3-iso-butylxanthine (IBMX] were compared in terms of purified cyclic GMP PDE inhibition. The relationship between the structure and inhibition of cyclic GMP PDE was studied. 3. The -log EC50 values for relaxation of spontaneous tone of isolated guinea-pig trachealis preparations by the 3-alkylxanthines and 1-methyl-3-alkylxanthines were determined. 4. The five 1-methyl-3-alkylxanthines were each more potent in relaxing isolated trachealis smooth muscle than the corresponding 3-alkylxanthines. The 1-methyl-3-alkylxanthines were also more potent than the corresponding 3-alkylxanthines in their cyclic GMP PDE inhibitory effect. There was a strong positive correlation between the concentration of inhibitor which inhibited hydrolysis by 50% (IC50) values for cyclic GMP PDE inhibition by the xanthine derivatives and their EC50 values for trachealis muscle relaxation. 5. It is suggested that the mechanism by which xanthine derivatives relax trachealis smooth muscle involves inhibition of cyclic GMP PDE in addition to inhibition of cyclic adenosine monophosphate PDE.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1991

Endocrine cells in a normal breast and non-cancerous breast lesion.

The authors confirmed the presence of endocrine cells for the first time in a normal breast as well as in a non-cancerous lesion of the breast. One hundred and eighty-eight blocks of normal breast tissues in 44 cases and 74 blocks of non-cancerous lesions in 35 cases were examined. Argyrophil cells were found in one block from a normal breast and in one block from a phyllodes tumor. Argyrophil cells in the normal breast showed positive reaction to anti-endocrine granule constituent (EGC) antibody with immunohistochemical method. Argyrophil cells found in the phyllodes tumor gave positive reaction to both anti-EGC and anti-serotonin antibodies. The present study is thought to be the first report in the literature of serotonin-positive cells in a non-cancerous breast lesion, a phyllodes tumor.

Adult↗
PubMed1991

Erythromycin reduces the severity of bronchial hyperresponsiveness in asthma.

It has been demonstrated that bronchial hyperresponsiveness is a characteristic feature of bronchial asthma, and airway inflammation plays an important role in bronchial hyperresponsiveness. Erythromycin is an antibiotic extensively used worldwide which is also reported to have anti-inflammatory action. This study was designed to clarify whether erythromycin could favorably alter bronchial responsiveness in patients with bronchial asthma. To estimate bronchial responsiveness, histamine challenge was performed in 23 patients with bronchial asthma (atopic type, 11; nonatopic type, 12). All patients were treated for ten weeks with erythromycin, 200 mg three times daily, orally. After ten weeks' treatment, PC20, an index of bronchial sensitivity, was increased significantly. There was no difference between atopic and nonatopic patients in the improvement of PC20. It was concluded that erythromycin reduces the severity of bronchial responsiveness in patients with bronchial asthma.

Adult↗
PubMed1991

Recovery time course of airway hyperresponsiveness to acetylcholine after ovalbumin challenge in guinea pigs.

Sequential changes in airway and adrenergic responsiveness after ovalbumin (OA) challenge were studied in guinea pigs. Airway responsiveness, alpha 1- and beta-adrenoceptor numbers and adenylate cyclase activity was determined after increasing doses of acetylcholine aerosol were administered before, 0, 3, 7, and 14 days after exposure to 2 percent OA or physiologic saline solution for 10 consecutive days. The antiasthmatic agent, azelastine (1 mg/kg/day, intraperitoneal), was administered for 14 days after the tenth exposure to OA in some animals. Airway responsiveness increased significantly after OA exposure, beta-adrenoceptor numbers decreased by 35 percent, and adenylate cyclase activity decreased by 54 percent (p less than 0.01). Values remained significantly different than control animals for 7 days and required 14 days to normalize completely. Azelastine decreased the recovery period to seven days. Azelastine may affect airway responsiveness, at least in part, by increasing beta-adrenergic responsiveness.

Acetylcholine↗
PubMed1991

Effect of erythromycin on bronchial hyperresponsiveness in patients with bronchial asthma.

The effects of erythromycin (erythromycin stearate, Erythromycin; CAS 643-22-1) on the bronchial hyperresponsiveness and the functions of lymphocytes and neutrophils were evaluated. Administration of erythromycin to asthmatic patients in a dosage of 600 mg/d for 10 weeks reduced the bronchial hyperresponsiveness measured by histamine inhalation test. Furthermore, incubation with erythromycin for 96 h inhibited the mixed lymphocyte reaction at the concentration of more than 10 mumol/l in a dose-dependent manner, and the value of IC50 was about 30 mumol/l. 2-h incubation with erythromycin showed a weak inhibition to n-formyl-methionyl-leucyl-phenylalanine (FMLP)-induced superoxide production of polymorphonuclear neutrophils (PMNs) at the concentration of more than 30 mumol/l in a dose-dependent manner. 1-h incubation with 1 mumol/l and 100 mumol/l of erythromycin inhibited FMLP-induced chemotaxis of PMNs. The rates of inhibition at the concentration of 1 mumol/l and 100 mumol/l were 29.7% and 41.7%, respectively. Erythromycin thus showed a beneficial effect on bronchial hyperresponsiveness. This effect might be due to the regulation of the inflammatory cells.

Adult↗
PubMed1991

[The effect of azelastine on the down-regulation of beta-adrenoceptors].

The effect of azelastine, a new on the down-regulation of beta-receptor agonist was investigated. Male Hartley guinea pigs received injections of saline or terbutaline (T.) and/or azelastine (A.) for successive 7 days. The radioligand binding assays for beta-adrenoceptors in the lung membranes of the guinea pigs were performed. The results showed the differences of numbers of maximal binding sites (Bmax) among four groups were significant. The Bmax of beta-adrenoceptor in T. group was less than that in control group (P less than 0.02). The Bmax in A. group was more than that in control group (P less than 0.05). The Bmax in T. plus A. was more than that in T. group, and there was no significant difference between Bmax in T. group and in T. plus A. group (P greater than 0.1). The differences of affinity (Kd) of beta-adrenoceptor among four groups were not significant. Azelastine increased the density of beta-adrenoceptors and partially prevented the down-regulation of beta-adrenoceptor caused by terbutaline.

Animals↗
PubMed1991

Effect of azelastine on the down regulation of beta-adrenoceptors in guinea pig lung.

The new antiallergic drug azelastine (E-0659, Azeptin; CAS 58581-89-8) is used in the treatment of rhinitis and bronchial asthma. In the present study, the effect of azelastine on the regulation of the beta-adrenoceptors and the down regulation of beta-adrenoceptors by terbutaline, a beta-agonist, was investigated using guinea pig lungs. Guinea pigs were divided into four groups; (1) the control (saline-treated) group, (2) the terbutaline-treated group, (3) the azelastine-treated group, (4) terbutaline plus azelastine-treated group. Guinea pigs intramuscularly injected with each agent three times a day for successive 7 days. In the terbutaline-treated group, a 26% reduction in the number of beta-adrenoceptors compared with those of the control group was observed. In the azelastine-treated group, the number of beta-adrenoceptors increased by 24% compared with those of the control group. The number of the beta-adrenoceptors in the terbutaline plus azelastine-treated group was significantly increased compared with that of the terbutaline-treated group. These results suggest that azelastine may prevent the down regulation observed during beta-agonist administration by increasing the number of beta-adrenoceptors.

Animals↗
PubMed1991

[Tumor necrosis factor in sputa of patients with bronchial asthma on exacerbation].

TNF is a cytokine recently implicated as an important inflammatory mediator. TNF concentrations in sputa from 13 patients with bronchial asthma on exacerbation and 12 patients with chronic obstructive pulmonary disease were measured. After sonication, the sputa were centrifuged. The supernatants were assayed for the presence of TNF by use of an enzyme-linked immunosorbent assay. TNF was detected in all patients with bronchial asthma (1783 +/- 420 pg/ml), while low values of TNF were detected in only 5 of the 12 COPD patients. It is suggested that TNF is involved in airway inflammation in bronchial asthma.

Acute Disease↗
PubMed1991

Inhibitory effect of dietary administration of eicosapentaenoic acid on the contractions of guinea-pig tracheal smooth muscle induced by leukotriene C4 and D4.

The changes in fatty acid composition in phospholipids of guinea-pig lung parenchymal strips and trachea induced by dietary administration of eicosapentaenoic acid (EPA) were investigated as well as the resultant changes in leukotriene (LT) C4- and D4-induced contractions of guinea-pig tracheal smooth muscle. EPA levels in both parenchymal strips and trachea were significantly increased depending on the administered dose of EPA, but on the other hand, arachidonic acid levels in those preparations were not changed. Both the contractions of guinea-pig tracheal smooth muscle induced by LTC4 and D4 were significantly reduced in the EPA-treated group compared with the control group at all 3 concentrations, 10(-9), 3 x 10(-9) and 10(-8) mol/l, in the presence of 5 x 10(-5) mol/l indometacin, a cyclooxygenase inhibitor. But this significant reduction of the contraction was not recognized between these 2 groups in the presence of 10(-5) mol/l 2-(12-hydroxydodeca-5, 10-diynyl)-3,5,6-trimethyl-1,4-benzoquinone (AA861), a 5-lipoxygenase inhibitor, or in the combined presence of 5 x 10(-5) mol/l indometacin and 10(-5) mol/l of AA861. These results suggest that: 1. a 5-lipoxygenase pathway is partly involved in the contractions of guinea-pig tracheal smooth muscle induced by LTC4 and D4 and; 2. EPA suppresses LTC4- and D4-induced contractions of guinea-pig tracheal smooth muscle through a 5-lipoxygenase pathway.

Animals↗
PubMed1991

[Roentgenographical evaluation of physiological bow-leg and the infantile type of Blount's disease in children].

Roentgenographical examinations were carried out in 41 joints of 22 cases with physiological bowleg and 7 joints of 5 cases with the infantile type of Blount's disease. The observation periods were from 1 year and 4 months to 8 years and 1 month with an average of 4 years and 2 months. The femorotibial angle, the proximal tibial metaphyseal diaphyseal angle, the distal tibial metaphyseal diaphyseal angle and the tibial metaphyseal metaphyseal angle were measured, and evaluated statistically. The measurement of the proximal tibial metaphyseal diaphyseal angle and the tibial metaphyseal metaphyseal angle were more significant than that of the femorotibial angle for early differentiation of the infantile type of Blount's disease from physiological bowleg. The degree and it's change of the distal tibial metaphyseal diaphyseal angle show no difference between physiological bowleg and the infantile type of Blount's disease.

Age Factors↗
PubMed1990

Alteration of 1,2-diacylglycerol content in ischemic and reperfused heart.

The myocardial 1,2-diacylglycerol (DG) and phospholipid levels during ischemia and reperfusion were studied in open-chest dogs by means of sequential epicardial minibiopsies, followed by quantification based on mass measurement technique. 1,2-DG level increased as early as 5 min after coronary ligation but decreased at 30 min. Also as early as 2 min after postischemic (35 min) reperfusion, 1,2-DG level increased transiently compared to pre-reperfusion level. Prazosin inhibited these changes significantly. A significant change in the incidence of reperfusion-induced ventricular tachycardia (VT) was not obtained in the prazosin-treated group. However, the 1,2-DG level 2 min after reperfusion was significantly higher in the ischemic myocardium developed reperfusion-induced VT than in the undeveloped one. Phospholipid levels remained unchanged during ischemia and reperfusion. These results suggest that alpha 1-adrenergic stimulation occurs early in ischemia and reperfusion and leads to 1,2-DG accumulation, which may be involved in the pathogenesis of ischemic and reperfusion injury.

Animals↗
PubMed1990

Neostigmine-induced hyperglycemia is mediated by central muscarinic receptor in fed rats.

We previously reported that neostigmine injected into the third cerebral ventricle stimulated adrenal secretion of epinephrine, secretion of glucagon from the pancreas, and direct neural innervation of the liver, resulting in hepatic venous plasma hyperglycemia in anesthetized fed rats. However, receptor type of these 3 mechanisms is not known. Therefore, we examined the effects of intraventricularly injected cholinergic or adrenergic antagonists on neostigmine-induced catecholamines in intact rats, glucagon secretion which is mediated by direct neural innervation of pancreas in bilateral adrenalectomized (ADX) rats, and hepatic venous hyperglycemia which is mediated by direct neural innervation of liver in ADX rats receiving constant infusion of somatostatin from femoral vein. Atropine injected into the third cerebral ventricle suppressed epinephrine secretion and dose-dependently inhibited hepatic venous hyperglycemia induced by neostigmine in intact rats. The neostigmine-induced glucagon secretion which occurs in ADX rats was suppressed by atropine. Atropine also prevented the neostigmine-induced hyperglycemia in ADX rats receiving constant somatostatin infusion through femoral vein (ADX-Somato rats). On the other hand, phentolamine, propranolol and hexamethonium showed no significant inhibitory effect on neostigmine-induced hyperglycemia, epinephrine and glucagon secretion in intact rats, glucagon secretion in ADX rats, or hyperglycemia in ADX-Somato rats. These results suggest that neostigmine-induced epinephrine and glucagon secretion and increased hepatic glucose output stimulated by direct neural innervation to liver is mediated by central muscarinic receptor in fed rats.

Adrenergic Fibers↗
PubMed1990

Isoenzyme profiles of creatine kinase, lactate dehydrogenase, and aspartate aminotransferase in the diabetic heart: comparison with hereditary and catecholamine cardiomyopathies.

STUDY OBJECTIVE: The aim was to investigate the redistribution of isoenzymes, clinically important markers of myocardial necrosis, in the diabetic heart and compare it with that investigated in other types of cardiomyopathies. DESIGN: Myocardial isoenzyme activity of creatine kinase (CK), lactate dehydrogenase (LD) and aspartate aminotransferase (AST) was measured in animals with diabetic, hereditary, and catecholamine cardiomyopathies. SUBJECTS: Diabetic rats (4 and 8 weeks after intravenous streptozotocin, n = 21), Bio 14.6 hamsters (30, 90, 160 and 240 days old, n = 29), and rats injected with isoprenaline (0.25, 0.5 and 1.0 mg.kg-1.d-1 for 3 weeks, n = 20) were used. Controls were age matched intact animals (n = 8-11). MEASUREMENTS AND MAIN RESULTS: Total CK and CK MM activity decreased in all groups. CK MB and BB decreased by 62 and 52% in diabetic rats, but increased by 40 and 33% in Bio hamsters and by 9 and 96% in isoprenaline treated rats. Thus the CK-B subunit decreased by 61% in diabetics and increased by 33 and 38% in Bio and isoprenaline groups, while the CK-M subunit decreased in all groups. Mitochondrial CK decreased in diabetic and isoprenaline groups. Total LD activity increased in diabetics and decreased in Bio. LD-H subunit increased by 21% in diabetics and decreased by 19 and 18% in Bio and isoprenaline groups. Accordingly the proportion of LD-M subunit, an index of anaerobic metabolism, decreased in diabetics and increased in Bio and isoprenaline groups. Changes in CK-M and CK-B subunits and the LD-M proportion in diabetic heart were normalised by insulin. Total AST activity decreased in diabetics because of the reduction in mitochondrial AST. CONCLUSIONS: Increased LD-M proportion and CK-B observed in Bio and isoprenaline groups may be a metabolic "compensation" to decreased myocardial perfusion and substrate. Decreased LD-M proportion and CK-B in the diabetic heart was insulin dependent and may indicate either lack of "compensation" to myocardial ischaemia or absence of ischaemia per se. Decreased myocardial CK and CK MB activity possibly causes underestimation of enzymatically assessed infarct size in the diabetic heart.

Animals↗