PubMed Health⌕ Search

Biomedical subjects

T Satake

Publications and source records attributed to T Satake.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1990

Comparison of theophylline and enprofylline effects on human neutrophil superoxide production.

1. We investigated effects of theophylline (widely used for the treatment of asthma) and enprofylline (a new xanthine derivative with negligible adenosine antagonism) on O2- production by human neutrophils with n-formyl-methionyl-leucyl-phenylalanine (FMLP) stimulation. 2. Therapeutic concentrations of theophylline (1-100 mumol/L) enhanced O2- production, maximally by 43.1 +/- 24.4% at 30 mumol/L; the same concentrations of enprofylline inhibited O2- production. 3. When each agent was administered after pre-incubation with adenosine deaminase (ADA) (0.1 U/mL), O2- production was inhibited in a concentration-dependent manner in comparison with that under administration of ADA alone. 4. These results suggest that the difference of effects in the two xanthine derivatives at therapeutic concentrations might be due to the presence or absence of adenosine antagonism.

Adenosine↗
PubMed1990

Time course of recovery of beta- and alpha 1-adrenoceptors in experimental asthma.

1. The time course of recovery of reduced beta-adrenoceptors caused by ovalbumin (OA) challenge was investigated using guinea-pigs. 2. The effects of prednisolone on the recovery time course were also evaluated. 3. beta- and alpha 1-receptor assays were performed using lung membranes. Adenylate cyclase activity was also measured. 4. OA challenge reduced the number of beta-adrenoceptors by 35%, and a significant decrease (13%) persisted for 7 days. The number of beta-adrenoceptor recovered after 14 days. 5. OA challenge elevated the number of alpha 1-adrenoceptors. A significant increase (24%) was observed after 7 days, and it took a further 7 days for the recovery. 6. After OA challenge there was a significant decrease in adenylate cyclase activity after 7 days, which recovered after a further 7 days. 7. Inhalation of prednisolone accelerated the recovery of beta-adrenergic responsiveness, though it did not affect the recovery of the number of alpha 1-adrenoceptors. Prednisolone inhalation also elevated beta-adrenergic responsiveness in non-asthmatic subjects. 8. It is concluded that reduced beta-adrenergic responsiveness caused by OA challenge persisted for 7 days and recovered after a further 7 days. Steroid hormone increased beta-adrenoceptors.

Adenylyl Cyclases↗
PubMed1990

Effects of intracellular pH on calcium-activated potassium channels in rabbit tracheal smooth muscle.

1. The effects of intracellular pH (pHi) on calcium-activated potassium channels (Ca2(+)-activated K+ channels) were studied in membrane patches of smooth muscle freshly dispersed from the rabbit trachea. Single-channel currents were recorded with an 'inside-out' patch clamp technique, mainly at 0 mV, with the external (electrode) medium containing 130 mM-K+ and the internal (bath) medium 6 mM-K+. 2. With an internal Ca2+ concentration ([Ca2+]i) of 1 microM, the fraction of time during which the channel was in an open state (the open probability, Po) was more than 0.8 at pHi 7.4. The channel activity nearly disappeared at pHi 7.0. The [Ca2+]i-Po relationship was shifted to higher [Ca2+]i by acidosis, the shift being approximately an 8-fold increase for a fall in pHi of 0.5 units. 3. The membrane potential and current intensity (V-I) relationship of single channels between +30 and -50 mV was shifted in a hyperpolarizing direction by intracellular acidosis. The shift was roughly 10 mV for 1 pH unit at 1 microM [Ca2+]i. At pHi 7.4 [Ca2+]i 1 microM, the V-Po relationship was shifted in a depolarizing direction by acidification. When [Ca2+]i was increased to 10 microM, V-Po relationship became less sensitive to V as well as pHi changes. 4. When Po was high, the probability density function of open and closed time distributions could be fitted by two exponentials. When Po was decreased to less than 0.3, either by reducing [Ca2+]i or by lowering pHi, another component having long closed times appeared. At similar Po values, the time constant of open time distribution was smaller with lower pHi. 5. It is concluded that the main effect of an increase in intracellular hydrogen ions is to decrease the open probability of the Ca2(+)-activated K+ channel, by reducing the sensitivity to Ca2+ and also shortening the open state.

Action Potentials↗
PubMed1990

Prostaglandin H2 may be the endothelium-derived contracting factor released by acetylcholine in the aorta of the rat.

The present experiment was performed to identify endothelium-derived contracting factor produced by acetylcholine stimulation in the aorta of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. The rings of the thoracic aorta were obtained from age-matched SHR and WKY rats, and changes in isometric tension were recorded. The relaxant responses to acetylcholine in the aortic rings from SHR were significantly weaker than those from WKY rats. The relaxant responses to acetylcholine were significantly enhanced by pretreatment with a cyclooxygenase inhibitor (indomethacin) or thromboxane A2/prostaglandin H2 receptor antagonist (ONO-3708) in aortic rings from both SHR and WKY rats. A thromboxane A2 synthetase inhibitor (OKY-046) did not affect the acetylcholine-induced relaxation in the aortic rings from SHR or WKY rats. In the organ bath solution, after acetylcholine stimulation, prostaglandin E2 and 6-keto-prostaglandin F1 alpha concentrations increased but not prostaglandin F2 alpha and thromboxane B2 concentrations. Exogenous prostaglandin H2, a stable analogue of thromboxane A2, and prostaglandin F2 alpha induced contractions of the SHR rings at a lower concentration than prostaglandin E2, prostaglandin D2, and prostaglandin I2. These contractile responses to various prostaglandins were markedly inhibited by pretreatment with ONO-3708. A prostacyclin synthetase inhibitor did not affect the relaxant responses to acetylcholine in the SHR rings. These results show that endothelium-derived contracting factor is produced and released by acetylcholine stimulation not only in the aorta of SHR but also in those of WKY rats and suggest that prostaglandin H2, a precursor of the released prostaglandins, is a strong candidate for endothelium-derived contracting factor produced by acetylcholine stimulation.

Acetylcholine↗
PubMed1990

Emphysematous change in chronic asthma in relation to cigarette smoking. Assessment by computed tomography.

To evaluate the occurrence and the degree of emphysema in chronic asthma in relation to the effect of cigarette smoking, we examined 35 subjects with irreversible airway obstruction (17 nonsmokers and 18 smokers). We performed pulmonary function testing and CT scans on all subjects. The ES was assessed by a visual scoring system on CT scans. Between nonsmokers and smokers, there was a significant difference in the ES (p less than 0.05), but not in the FEV1, TLC, and Dsb/VA (expressed as percent predicted values). The ES was 2.3 +/- 4.7 percent (mean +/- SD) in nonsmoking subjects and 13.7 +/- 16.7 percent in smoking subjects. In all subjects the ES showed significant correlations with Dsb/VA (p less than 0.001) and pack-years of cigarette consumption (p less than 0.001) but did not show correlations with FEV1 and with TLC. We concluded that emphysema can occur in smoking asthmatic subjects because of the effect of cigarette smoking, and CT scans are useful for detecting this emphysematous change.

Asthma↗
PubMed1990

Effect of thyroxine injection on bone growth in energy deficient rats.

We investigated the role of thyroxine on bone growth in energy deficient rats. Rats were fed a normal diet and injected with saline, or a low-energy diet and injected with saline or 0.1, 1, or 5 micrograms/100 g BW of thyroxine for 22 days. Thyroxine injections decreased body weight gain but did not affect bone length and width. The epiphyseal growth plate was thinner and the activities of bone alkaline and acid phosphatase in energy deficient and 5 micrograms/100 g BW thyroxine injected animals were lower than that of the other treatment groups. Serum total thyroxine and triiodothyronine concentrations were increased but somatomedin C concentration was decreased by injecting with 5 micrograms/100 g BW of thyroxine in energy deficient rats.

Acid Phosphatase↗
PubMed1990

Priming effect of recombinant human interleukin-2 and recombinant human interferon-gamma on human neutrophil superoxide production.

The effect of recombinant human interleukin-2 (rhIL-2) and recombinant human interferon-gamma (rhIFN-gamma) were evaluated on superoxide (O2-) production of human polymorphonuclear neutrophils (PMNs). Ten minutes incubation with rhIL-2 showed a dose-dependent enhancement of n-formyl-methionyl-leucyl-phenylalanine (FMLP)-induced O2-production of human PMNs, and the rate of enhancement reached 49.6% at the concentration of 3000 U/ml rhIL-2. Same pretreatment with rhIFN-gamma also showed a dose-dependent enhancement of FMLP-induced O2-production of human PMNs, and the maximal rate of enhancement was 47.0% at the concentration of 3000 U/ml rhIFN-gamma. Any cytokines given alone did not induce O2- production. These cytokines showed no enhancement of phorbol myristate acetate (PMA)-induced O2- production, neither. The effects of these cytokines to FMLP-induced O2- production were kept in calcium-free medium. Moreover, incubation with these cytokines caused no elevation of intracellular free calcium concentration [( Ca++]i) in resting PMNs. Incubation with them did not change the increase of [( Ca++]i) of PMNs induced by FMLP significantly, neither. Recombinant forms of cytokines are used clinically, now. These results may be helpful for the use of them.

Adult↗
PubMed1990

Mechanism of atrial natriuretic polypeptide and sodium nitroprusside-induced relaxation in guinea-pig tracheal smooth muscle.

Atrial natriuretic polypeptide (ANP) is composed of a family of peptides isolated from rat and human atria. In the present study, the relaxant effects of ANP, sodium nitroprusside and 8-bromo-cyclic guanosine monophosphate (GMP) were investigated in guinea-pig tracheal smooth muscle, and the tissue cyclic GMP and cyclic adenosine monophosphate (AMP) concentrations were measured. ANP, sodium nitroprusside and 8-bromo-cyclic GMP showed relaxant effects on the spontaneous tone in normal Krebs solution (5.9 mmol/l K(+)-2.4 mmol/l Ca++ solution). They diminished relaxant effects on 40 mmol/l K(+)-0.1 mmol/l Ca++ induced contraction, which was approximately the same tension as the spontaneous tone. Sodium nitroprusside and 8-bromo-cyclic GMP diminished less relaxant effects on 40 mmol/l K(+)-2.4 mmol/l Ca++ induced contraction, but ANP showed no relaxation. The tissue cyclic GMP levels following administration of ANP and sodium nitroprusside in normal Krebs solution, in 40 mmol/l K(+)-2.4 mmol/l Ca++ solution, and in 40 mmol/l K(+)-0.1 mmol/l Ca++ solution increased dose-dependently without regard to external Ca++ concentrations, while the tissue cyclic AMP levels did not change. These results suggest that ANP might be a novel potent relaxant in airway smooth muscle and the relaxant effect may be, at least in part, mediated by cyclic GMP. There was a difference in relaxant effects on tracheal smooth muscle between ANP and sodium nitroprusside.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

[Effect of pulsed electromagnetic fields (PEMF) on osteoblast-like cells. Alterations of intracellular Ca2+].

Low-energy electromagnetic fields pulsed at frequencies of 60-90 Hz significantly increase healing of chronic fracture nonunions in man. These fields are effective at tissue current levels as low as several orders of magnitude lower than those required for transmembrane depolarization of normal cells. In this study, the effects of PEMF on culture of rat osteoblast-like cells have been examined. The PEMF promoted the growth of these cells, were also found to increase the basal level of [Ca2+]i, and to decrease the responses towards epidermal growth factor (EGF) and serum, when the degree of response was based on the intracellular Ca2+ transient. These effects of PEMF were mimicked by 12-O-tetradecanoyl phorbol 13-acetate (TPA), a potent activator of protein kinase C. Pretreatment of TPA enhanced the cell growth and suppressed the intracellular Ca2+ transient induced with EGF and then serum to about 170% of the control. Then, present study investigated how the PEMF and TPA modulate EGF receptors of these cells. Both PEMF and TPA decreased the level of EGF binding to these cells down to about 65% and 75%, respectively. Scatchard analysis revealed the decrease of EGF receptor without a significant change in the affinity for EGF by both. In conclusion, it was indicated that PEMF acts at cell membrane and modulates the receptors which is essential for cell growth and DNA synthesis.

Animals↗