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Biomedical subjects

T Satake

Publications and source records attributed to T Satake.

At least 91 records · Page 5Linked to original sources
PubMed1989

Protective effects of a thromboxane synthetase inhibitor, a thromboxane antagonist, a lipoxygenase inhibitor and a leukotriene C4, D4 antagonist on myocardial injury caused by acute myocardial infarction in the canine heart.

We studied the effects of a thromboxane A2 synthetase inhibitor (RS-5186), a thromboxane A2 antagonist (ONO-3708), a 5-lipoxygenase inhibitor (AA-861) and a peptidoleukotriene antagonist (ONO-1078) on infarct size, polymorphonuclear leukocyte infiltration, gross myocardial hemorrhage and arrhythmias in the canine coronary occlusion (2 hour)-reperfusion model (5 hour). The infarct size and risk area were determined by a double staining technique. Thirty minutes prior to occluding the coronary arteries, dogs were randomly assigned to one of the following five groups: the thromboxane A2 synthetase inhibitor group (n = 11) receiving RS-5186 10 mg/kg i.v., the thromboxane A2 antagonist group (n = 12) receiving continuous intravenous infusion of ONO-3708 1 microgram/kg/min, the lipoxygenase inhibitor group (n = 11) receiving AA-861 3 mg/kg i.v., the peptidoleukotriene antagonist group (n = 11) receiving continuous intravenous infusion of ONO-1078 1 microgram/kg/min and the vehicle control group (n = 15). Except for ONO-3708, all the other drugs reduced the infarct size (RS-5186: 26.3 +/- 2.4% of risk area (mean +/- SEM), AA-861: 21.8 +/- 1.3%, ONO-1078: 22.5 +/- 4.4% vs control: 54.0 +/- 6.4%, p less than 0.01 respectively) as well as reducing the area of gross myocardial hemorrhage (RS-5186: 3.9 +/- 2.6% of infarct size, AA-861: 5.1 +/- 2.4%, ONO-1078: 5.2 +/- 2.5% vs control: 22.3 +/- 3.9%, p less than 0.01 respectively). RS-5186 and AA-861 reduced the intensity of polymorphonuclear leukocyte infiltration into the infarcted area, however, neither ONO-3708 nor ONO-1078 had any significant influence.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of azelastine, an antiasthmatic drug, on bronchial responsiveness in patients with bronchial asthma.

This study was designed to clarify whether azelastine, an antiasthmatic drug, could favorably alter bronchial responsiveness in patients with bronchial asthma. To estimate bronchial responsiveness, methacholine challenge was performed in 21 patients with bronchial asthma. After the first examination, all patients were treated for eight weeks with azelastine, 2 mg twice daily. After four and eight weeks' treatment, methacholine challenge was repeated. After eight weeks' treatment, Dmin, an index of bronchial sensitivity, was increased significantly, and after four weeks an insignificant increase was observed. The RrsC, SGrs/GrsC, indices of respiratory resistance and bronchial reactivity, respectively, did not change significantly during eight weeks' treatment. Recently various chemical transmitters, especially leukotrienes, were shown to be closely related to the genesis of bronchial asthma. Accordingly, the effect of azelastine observed here might be ascribed to its antagonizing action on leukotriene. Since bronchial hyperresponsiveness is a critical etiologic factor in bronchial asthma, long-term administration of azelastine might help to modify the disease's basic pathophysiologic conditions.

Adult↗
PubMed1989

Altered acetylcholine and norepinephrine concentrations in diabetic rat hearts. Role of parasympathetic nervous system in diabetic cardiomyopathy.

The concentrations of acetylcholine (ACh) as a parasympathetic marker and norepinephrine (NE) as a sympathetic marker were investigated in the hearts of rats 2, 4, and 8 wk after the induction of diabetes by an injection of streptozocin (STZ; 65 mg/kg i.v.). ACh and NE were measured by high-performance liquid chromatography with electrochemical detection. Diabetic rats showed low body weight and heart weight at 2, 4, and 8 wk and higher heart-to-body weight ratio and bradycardia at 8 wk, almost all of which were normalized after insulin treatment. Myocardial ACh and NE concentrations in the diabetic rats at 2 and 4 wk were not significantly different from those in age-matched control rats. However, ACh and NE concentrations in the diabetic rats at 8 wk significantly increased compared with the control rats. Diabetic rats at 8 wk also had increased myocardial choline concentration and choline acetyltransferase activity and decreased acetylcholinesterase activity. Insulin treatment normalized all of these changes in the diabetic rats. Thus, in STZ-induced diabetes (STZ-D), the concentrations of both cholinergic and noradrenergic neurotransmitters in the myocardium increased. The results of this study confirm a previously reported increase in sympathetic activity to the heart and also indicate that there is an increase in the synthesis and a decrease in the metabolism of ACh in STZ-D and that adequate insulin treatment normalizes these changes.

Acetylcholine↗
PubMed1989

Effects of digoxin on acetylcholine and norepinephrine concentrations in rat myocardium.

The influence of digoxin on the autonomic nervous system was studied in rats by examining its effects on the levels of acetylcholine (Ach), a parasympathetic marker, and norepinephrine (NE), a sympathetic marker, in the rat myocardium. Ach and NE were measured by high performance liquid chromatography with electrochemical detection (HPLC-ECD). Digoxin was injected subcutaneously every day for 4 weeks. The administration of 0.35, 0.75, and 2.5 mg/kg of digoxin reduced Ach concentrations in the right atrium to about 80-90% of the control value. However, there was no change in the activity of choline acetyltransferase (ChAT) or acetylcholinesterase (AchE), or in the concentration of choline (Ch). Injection of 0.1 mg/kg of digoxin had no significant effect on Ach concentration. When 0.75 and 2.5 mg/kg of digoxin were injected, there was a significant increase in NE concentration in the right atrium. Neither 0.1 nor 0.35 mg/kg caused any changes. Digoxin (0.75 and 2.5 mg/kg) increased heart rate to about 110% of the control values. Thus, high doses of digoxin increase the NE concentration but decrease the Ach concentration in the rat heart, and these changes might be related to functional changes in the autonomic nervous system.

Acetylcholine↗
PubMed1989

Effect of ibudilast on mucociliary transport using frog palate.

For the determination of mucociliary transport, we have used a method to measure mucociliary transport force (MCTF), which was defined as the tension developed by the mucus flow and ciliary motility of a frog palate between a force transducer and a glass boat on the palate. 3-isobutyryl-2-isopropylpyrazolo [1,5-a] pyridine (ibudilast) is supposed to increase intracellular cyclic adenosine monophosphate (cAMP) level by the inhibition of cAMP phosphodiesterase and to potentiate the effect of prostacyclin. The effect of ibudilast on MCTF was investigated for 15 min after the drug application. Ibudilast induced a significant, dose-related increase in MCTF at concentrations of higher than 10(-7) M. Therefore, these results indicate that ibudilast, an anti-allergic agent, activates mucociliary transport in respiratory tract.

Animals↗
PubMed1989

[Application of HPLC to measurement of plasma histamine in bronchial asthma].

We measured the plasma histamine concentration in patients with bronchial asthma by the post-column derivatization method developed by Yamatodani. The mean fasting plasma concentrations of histamine determined for bronchial asthma and control groups (male and female) were 1.93 +/- 0.29 (male) and 1.37 +/- 0.15 (female) pmol/ml and 4.05 +/- 0.69 (male) and 5.19 +/- 0.35 (female) pmol/ml, respectively. The histamine concentrations in the bronchial asthma group were significantly lower than those in the control group, although no significant sex-related difference was found. On the other hand, the histamine concentrations in the patients with bronchial asthma after provocation with histamine were significantly higher than when the patients were in a quiescent stable. In this study we can get the behavior of the slight changes in bronchial asthma by considering the finding for the patients, sampling trials and selection of the determination method.

Adult↗
PubMed1989

[Strongyloidiasis following long-term corticosteroid therapy].

A 64-year-old man who was born and raised in Fukuoka Prefecture was admitted because of dyspnea. The chest X-ray film showed multiple pulmonary cysts. Corticosteroid therapy was given because of repeated episodes of dyspnea and wheezing. He complained of epigastric pain 20 months after administration of corticosteroid therapy. Gastro-endoscopic examination showed inflammatory changes of the gastric mucosa and the biopsy specimens revealed the filariform larvae of Strongyloides stercoralis. Furthermore, the larvae were frequently detected in both sputum specimens and stools. Pyrvinium pamoate was initially administered and was switched to thiabendazole because of the presence of hyperinfection. Although two cycles of thiabendazole treatment were given, the larvae were not eradicated. This case report suggests that long term corticosteroid therapy caused the hyperinfection syndrome of Strongyloides stercoralis in a patient who was auto-infected with this nematode.

Adrenal Cortex Hormones↗
PubMed1989

[Increased neutrophils in bronchoalveolar lavage fluid from a patient with developing adult respiratory distress syndrome].

A 16-year-old, 28-week pregnant woman was admitted to our hospital with multiple bone fractures caused by a traffic accident. She had massive blood transfusion because of anemia in her laboratory findings and ritodrine hydrochloride was administered because of the fear of threatened abortion. She developed a cough with bloody sputum on the 4th day after admission, and developed pulmonary insufficiency with PaO2 41.0 torr and presented bilateral diffuse infiltrates on chest roentgenograms on the next day. Swan-Ganz catheterization revealed normal pulmonary capillary wedge pressure and analysis of the lavage fluid from the patient showed an increase in the percentage of neutrophils (40.0%) and the existence of leukotriene B4 which is known to be the most potent chemokinetic and chemotactic agent for neutrophils. Her condition was considered to be permeability edema developing adult respiratory distress syndrome (ARDS) and 1 g/day of methylprednisolone was administered intravenously for 3 days, which brought about remarkable improvement of her respiratory failure. This report suggests that analysis of the lavage fluid may provide useful information for the early diagnosis of ARDS and the indications of corticosteroid treatment.

Adolescent↗
PubMed1989

[TMJ clicking sounds and changes in masking level].

It is known that the peak distribution of the power spectrum seen in the clicking sounds of the temporomandibular joints appears in the vicinity of 1 KHz in a high rate. Based on the findings that this marginal zone corresponds to speech range, the authors have performed masking experiment by narrow band noise on 20 ears in 10 normal persons and 27 ears in 19 patients with noise as subjects to assess the influence exerted by mechanical stimulation on the condition of hearing ability in speech range. The results in normal persons were 14.8dB (S.D. 13.7) at 500Hz. 27.0dB (S.D. 11.1) at 1,000Hz and 21.3dB (S.D. 10.4) at 2,000Hz. The results in abnormal persons were 12.2dB (S.D. 9.9) at 500Hz, 20.6dB (S.D. 6.6) at 1,000Hz and 15.9dB (S.D. 4.4) at 2,000Hz. A significant difference was observed in the masking level between the two groups at 1,000Hz band with a risk rate of 5%. From the above, it was suggested that the sound constituent of TMJ clicking sound exerts influence on the specific auditory level in the patients with noise.

Hearing↗
PubMed1989

Changes in endogenous prostaglandin levels during D-galactosamine-induced liver injury.

The role of prostaglandins (PGs) in liver injury induced by D-galactosamine was investigated in the rat. The contents of PGD2 and PGF2 alpha in the liver were significantly increased from 3 h and 24 h after the D-galactosamine administration, respectively, but that of PGE2 was not significantly changed. Administration of 16,16-dimethyl PGE2, a long acting derivative of PGE2, or indomethacin, but not 16,16-dimethyl PGF2 alpha, a long acting derivative of PGF2 alpha, significantly depressed the increase in the serum transaminase activities induced by D-galactosamine. The protective effect of indomethacin was not disturbed by the 16, 16-dimethyl PGF2 alpha administration. These results indicate that PGE2 has a cytoprotective effect against the D-galactosamine induced liver injury and suggest that the protective effect of indomethacin is ascribable to its suppression of synthesis of PGs other than PGE2 or PGF2 alpha, e.g., PGD2.

Animals↗
PubMed1988

Detection of myocardial reperfusion by analysis of serum creatine kinase isoforms.

Serum creatine kinase (CK) MM isoforms were determined by chromatofocusing in 22 patients with acute myocardial infarction undergoing intracoronary thrombolysis. In 13 patients with successful coronary recanalization within 3.6 +/- 1.0 (SD) h after onset, time to peak CK activity occurred 13 +/- 3 h after onset which was significantly shorter (p less than 0.01) than that in 9 patients without coronary recanalization (20 +/- 4 h). The proportion of CK MM-A, the myocardial isoform, in serum in the reperfused group at 6, 10, and 14 h after onset (53 +/- 9, 38 +/- 5, and 27 +/- 4%, respectively) was always significantly lower (p less than 0.01) than that in the nonreperfused group (69 +/- 7, 59 +/- 8, and 43 +/- 4%). During the same period, the proportions of CK MM-B and CK MM-C, the converted isoforms derived intravascularly from MM-A by circulating carboxypeptidase, in the reperfused group were always significantly higher (p less than 0.01) than those in the nonreperfused group. The ratios of MM-A% to MM-B% and MM-A% to MM-C% amplified the differences between the two groups. At 10 h after onset, these ratios clearly differentiated the reperfused and the nonreperfused group at the values of 1.0 (MM-A/MM-B) and 3.0 (MM-A/MM-C) with the diagnostic sensitivity of 85% and 92%, respectively. Thus, myocardial reperfusion was detectable noninvasively by analysis of serum CK MM isoforms during the early stage of acute myocardial infarction.

Aged↗
PubMed1988

The role of phospholipase in plasmocid-induced mitochondrial dysfunction in rat hearts.

This study was designed to clarify the role of phospholipase in the mechanism of plasmocid-induced mitochondrial dysfunction in the rat heart. Rats were divided into two groups: the control group, untreated; and the plasmocid group, in which plasmocid (30 mg/kg) was injected subcutaneously. In each group, the level of lipid peroxides and the phospholipase activity in heart homogenate were measured, and mitochondrial function (respiratory control index and the rate of oxygen consumption in State III) was determined polarographically. The activity of lysosomal enzymes (N-acetyl-beta-glucosaminidase and beta-glucuronidase) were also measured. The plasmocid group showed significant increases in lipid peroxide levels and phospholipase activity. Administration of plasmocid also caused mitochondrial dysfunction, while no significant changes were observed in the lysosomal enzyme activity of either group. These results suggested that plasmocid-induced mitochondrial dysfunction is based on the degrading of phospholipids by membrane bound phospholipase, and that lysosomal enzymes are unlikely to be involved in plasmocid-induced mitochondrial dysfunction.

Acetylglucosaminidase↗
PubMed1988

Effects of atrial natriuretic polypeptide and organic nitrates on levels of relaxation and cyclic nucleotide of canine coronary artery with and without endothelial injury.

We studied the effects of organic nitrates and human atrial natriuretic polypeptide (hANP) on relaxation and tissue cyclic guanosine monophosphate (cGMP) levels using isolated canine coronary arteries with and without endothelial injury. Glyceryl trinitrate (GTN), isosorbide dinitrate (ISDN), pentaerythritol tetranitrate (PETN), and hANP relaxed both the injured and control coronary arteries, and they increased tissue cGMP levels in a dose-dependent fashion without changing tissue adenosine 3':5'-cyclic phosphate (cAMP) levels. The extent of relaxation was larger and the increase in cGMP was greater in the injured coronary artery than in the control artery. Methylene blue inhibited relaxation induced by GTN and hANP, and decreased tissue cGMP levels in both the injured and control groups. M&B 22,948 enhanced relaxation induced by GTN and hANP and increased tissue cGMP levels in both groups. The results suggest that organic nitrates and hANP relax the coronary artery by directly activating the guanylate cyclase in coronary smooth muscle and that such activation is independent of the endothelium-dependent vasodilator system.

Animals↗
PubMed1988

Effects of a new thromboxane A2-antagonist (ONO-3708) and a new leukotriene-antagonist (ONO-1078) on thromboxane A2 analogue-, leukotriene C4-, and D4-induced regional myocardial blood flow reduction.

Effects of the administration of a thromboxane A2 (TXA2) analogue (STA2), a leukotriene C4 (LTC4), and a leukotriene D4 (LTD4) on regional myocardial blood flow (RMBF) and hemodynamics were studied in anesthetized, open-chest dogs. The blocking ability of a recently synthesized TXA2 selective antagonist, ONO-3708, and a peptidoleukotriene-selective antagonist, ONO-1078, was also investigated. RMBF was measured continuously in three areas: the left anterior descending coronary artery (LAD) area, the circumflex artery (Cx) area, and the area between LAD and Cx. STA2, LTC4, and LTD4 caused a significant dose-dependent reduction of the RMBF in the LAD area. The peak percentage decrease in RMBF followed by a 10 micrograms dose of STA2, 1 micrograms dose of LTC4, and 1 micrograms dose of LTD4 is 38.6% +/- 3.0%, 39.0% +/- 3.1%, and 36.2% +/- 2.4%, respectively. ED50 for the action of LTC4, LTD4, and STA2 on RMBF is 3, 3, and 50 micrograms, respectively. Pretreatment with the newly developed TXA2 antagonist, ONO-3708 (1 micrograms/kg/min for 10 min), completely inhibited the RMBF reduction induced by STA2 (10 micrograms). Pretreatment with the peptidoleukotriene antagonist, ONO-1078 (1 mg), inhibited the RMBF reduction induced by LTC4 or LTD4 (0.3-3 micrograms). Following pretreatment with a 1 mg dose of ONO-1078, the peak percentage decrease of RMBF caused by a 1 micrograms dose of LTC4 and LTD4 was reduced to 21.1% +/- 2.3% and 19.8% +/- 3.1%, respectively. However, the LTC4 (1 micrograms)-induced reduction of the RMBF was not affected by pretreatment with a TXA2 antagonist, ONO-3708, or an inhibitor of the endogenous production of TXA2, OKY-046.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Quantitation of 1,2-diacylglycerol in rat heart by iatroscan TLC/FID.

1,2-Diacylglycerol, which has been recognized as one of the intracellular second messengers, was measured quantitatively in the lipid extract from rat hearts using the thin layer chromatography and flame ionization detection (TLC/FID) method. Cholesterol acetate was added to the tissue as an internal standard, and the crude lipids from the tissue were purified with silicic acid column to eliminate phospholipids. Development of Chromarods was carried out using two solvent systems and a three-step development technique. The relationship of the peak area ratio detected by flame ionization detector to weight ratio was linear compared with cholesteryl acetate. The 1,2-diacylglycerol content in the rat heart in the unstimulated condition was 72.5 +/- 15.3 ng/mg wet wt (mean +/- SD).

Animals↗
PubMed1988

Effect of the calcium antagonist, diltiazem, on beta-agonist-induced reduction of beta-adrenergic responsiveness in the guinea pig lung.

This study was designed to clarify the mechanism of tolerance that occurs during prolonged administration of a beta-agonist in relation to membrane phospholipid degradation and to elucidate the effect of diltiazem, a calcium antagonist. Guinea pigs were divided into 3 groups: (1) control--physiological saline (0.5 ml) was injected once a day for 7 successive days: (2) metaproterenol (Mp)--Mp was injected intraperitoneally (10 mg/kg/day) for 7 successive days: (3) Mp + diltiazem--diltiazem was injected intraperitoneally (20 mg/kg/day) 30 min before Mp injection for 7 successive days. The number of beta-adrenoceptors and the 10(5)M (-)-isoproterenol-stimulated adenylate cyclase activity were significantly decreased in the metaproterenol group. Diltiazem reduced these decreases. Phospholipase activity was increased and phosphatidylcholine and phosphatidylethanolamine levels were decreased in the metaproterenol group. Diltiazem also reduced these changes. These results suggest that the degradation of membrane phospholipids by phospholipase may be involved in a decrease in beta-adrenergic response caused by successive administration of metaproterenol. Diltiazem protects membrane phospholipids from phospholipase attack, which in turn maintains beta-adrenergic responsiveness.

Adenylyl Cyclases↗
PubMed1988

Neutrophil-derived epoxide, 9,10-epoxy-12-octadecenoate, induces pulmonary edema.

We have observed that neutrophils biosynthesize linoleate epoxide, 9,10-epoxy-12-octadecenoate, and have named it leukotoxin because of its cytotoxic effect. In this experiment, the effect of leukotoxin on the lung was investigated. Acute effect of leukotoxin: Using Wistar rats, leukotoxin (100 mumol/kg) was injected intravenously for the leukotoxin group, and linoleate (100 mumol/kg) for the linoleate group. Physiological saline was injected as the control. Ten min after injection, rats were divided into 3 groups: (1) lungs were isolated, and lung wet weight, and dry weight were measured; (2) lung lavages were performed, and albumin concentration and activity of angiotensin converting enzyme (ACE) were measured; (3) morphological changes were studied by light and electron microscope. After administration of leukotoxin, lung wet weight/body weight ratios and dry weight/wet weight ratios were increased. Albumin concentration and ACE activity in lung lavages were also increased. Pulmonary edema was also confirmed by light microscopic findings. Alveolar epithelial cell damage and endothelium damage were also observed. Linoleate had no significant effect on these biochemical parameters and morphological findings. Subacute effect of leukotoxin: Twelve hr after administration of leukotoxin (50 mumol/kg) or linoleate (50 mumol/kg), the same studies were performed as in the acute experiments. Immediately after administration of leukotoxin, no significant effect was observed. However, 12 hr later similar changes were observed as in the acute experiments. Linoleate did not show any significant effect 12 hr after injection. These results indicate that leukotoxin biosynthesized by neutrophils might be closely related to the genesis of inflammatory edema.

Animals↗