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Biomedical subjects

Y Fujise

Publications and source records attributed to Y Fujise.

At least 19 recordsLinked to original sources

The roles of platelet-activating factor and endothelin-1 in renal damage after total hepatic ischemia and reperfusion.

BACKGROUND: This study was designed to verify the involvement of platelet-activating factor (PAF) in renal damage associated with hepatic ischemia and reperfusion (HIR) injury through the release of endothelin (ET)-1 and to determine the modulating effect of a specific PAF receptor antagonist on these insults in rats. METHODS: Male rats pretreated with either normal saline as a vehicle (NS group) or intravenous TCV-309, a PAF receptor antagonist (TCV group), were subjected to 120 min of total hepatic ischemia under an extracorporeal portosystemic shunt. Plasma aspartate transaminase, creatinine, blood urea nitrogen, and ET-1 levels and the relative renal wet weight were determined under nonischemic conditions and at 1, 3, and 6 hr of reperfusion after hepatic ischemia. Changes in mean arterial blood pressure and renal tissue blood flow measurements in the kidney were determined throughout the experiment. RESULTS: Increased plasma aspartate transaminase, creatinine, blood urea nitrogen, and ET-1 levels and the relative renal wet weight after HIR in the NS group were significantly suppressed by TCV-309 pretreatment. Mean arterial blood pressure and renal tissue blood flow after HIR in the TCV group were significantly improved when compared with those in the NS group. These effects resulted in attenuation of structural hepatic and renal damage with the improvement of 7-day survival (62%). CONCLUSIONS: The present study demonstrates that renal damage as well as critical liver injury is produced after reperfusion following 120 min of total hepatic ischemia. A PAF receptor antagonist may be therapeutically useful to protect against these types of damage via indirect modulation of plasma ET-1 levels.

Animals↗

Macromolecular surfactant as a pseudo-stationary phase in micellar electrokinetic capillary chromatography.

We examined polymers of sodium 11-acrylamidoundecanoate [poly(Na 11-AAU)] with a very high molecular mass (>10(6)) for their potential use as a pseudo-stationary phase in micellar electrokinetic capillary chromatography (MEKC). Size-exclusion chromatography and capillary electrophoresis studies reveal that the polymers are highly charged, and have a densely packed chain structure. For aromatic compounds, the polymeric surfactant showed significantly different selectivity than sodium dodecyl sulfate (SDS). It was suggested that one molecule of poly(Na 11-AAU) forms one micelle. The structural stability of this pseudo-stationary phase permitted its use with relatively high percentages of organic modifiers in the buffer medium, allowing the separation of highly hydrophobic compounds which are difficult to analyze by conventional MEKC with SDS.

Chromatography, Micellar Electrokinetic Capillary↗

Role of high-energy phosphate metabolism in hydrogen peroxide-induced cardiac dysfunction.

This study was undertaken to clarify the role of high-energy phosphate metabolism in hydrogen peroxide-induced cardiac dysfunction using phosphorus and fluorine nuclear magnetic resonance spectroscopy. The exposure of a Langendorff-perfused heart to hydrogen peroxide (200-400 micromol/L, 8 min) provoked biphasic contractile dysfunction characterized by a transient depression of left ventricular developed pressure during the administration of hydrogen peroxide and a delayed elevation of left ventricular end-diastolic pressure after the washout of hydrogen peroxide. The initial phase of cardiac dysfunction correlated well with the accumulation of sugar phosphates (r = 0.89, p < 0.01). Furthermore, we demonstrated that glibenclamide, a potent inhibitor of the ATP-sensitive K+ channel, attenuated the initial depression of developed pressure. On the other hand, the delayed elevation of end-diastolic pressure correlated well with the total ATP depletion (r = 0.96, p < 0.01). However, ATP loss was supposed to be a mere result from the increased ATP consumption corresponding to a rise in intracellular free Ca2+ (from the control value of 315+/-23 nmol/L to 708+/-104 after the administration of hydrogen peroxide, p < 0.01), which also paralleled the elevation of end-diastolic pressure. Thus glycolytic inhibition and intracellular Ca2+ overload are independently responsible for the biphasic contractile dysfunction induced by hydrogen peroxide.

Adenosine Triphosphate↗

Effects of an endothelin receptor antagonist TAK-044 on myocardial energy metabolism in ischemia/reperfused rat hearts.

The purpose of this study was to investigate the effects of an endothelin-receptor antagonist TAK-044 on functional defects and metabolic derangement in myocardial ischemia/reperfusion injury. We sequentially measured high-energy phosphate metabolites and intracellular pH by phosphorus magnetic resonance spectroscopy during 35-min global ischemia followed by 60-min reperfusion in Langendorff-perfused rat hearts. TAK-044 (initial loading by 3 mg/kg followed by perfusion with 100 nM solution) was administered in two different ways: before ischemia or immediately after reperfusion. In addition, we investigated the effects of TAK-044 on functional defects and metabolic alterations induced by hydrogen peroxide (200 microM, 30 min). The recoveries of left ventricular developed pressure after reperfusion in TAK-044 groups (51 +/-12% in TAK-I, 61 +/- 12% in TAK-R) were better than in control (10 +/- 5% in control; p < 0.01). Increases in left ventricular end-diastolic pressure (LVEDP) in TAK-044 groups (22 +/- 5 mm Hg in TAK-I, 24 +/- 5 mm Hg in TAK-R) were less than in control (38 +/- 3 mm Hg; p < 0.01). Adenosine triphosphate (ATP) (33 +/- 5% in TAK-I, 28 +/- 4% in TAK-R) in TAK-044 groups were higher than in control (13 +/- 3%; p < 0.01). The creatine phosphokinase (CPK) release during reperfusion in TAK-044 groups (3.3 +/- 1.5 IU/g wet wt/60 min in TAK-I, 3.5 +/- 2.5 IU/g wet wt/60 min in TAK-R) were lower than in control (13.8 +/- 3.9 IU/g wet wt/60 min; p < 0.05). In contrast, TAK-044 did not attenuate the myocardial injury induced by hydrogen peroxide. TAK-044, even if administered simultaneous with coronary reperfusion, attenuated myocardial ischemia/ reperfusion injury. The energy-preservative effect of TAK-044 could be associated with the good functional recovery in ischemia/reperfused rat hearts.

Animals↗

Giant noninflammatory and nonatherosclerotic coronary arterial aneurysm in the left main trunk assessed by intravascular ultrasound imaging--a case report.

A case of a giant noninflammatory and nonatherosclerotic coronary arterial aneurysm in the left main trunk of a 69-year-old female is reported. Preoperative intravascular ultrasound (IVUS) images were helpful for visualizing the morphologic and histologic features of the coronary aneurysm. They were also useful for determining the etiologic background and surgical procedure.

Aged↗

Evaluation of the effects of photodynamic therapy with phosphorus 31 magnetic resonance spectroscopy.

Magnetic resonance spectroscopy in situ was used to study changes in phosphorus 31 metabolism after photodynamic therapy (PDT) of transplanted HeLa cell tumours. Tumours were irradiated 2 h after administration of ATX-S10 (8-formyloximethylidene-7-hydroxy-3-ethenyl-2,7,12,18, tetramethyl-porphyrin-13,17-bispropionil aspartate), a new photosensitizer and chlorin derivative. Nuclear magnetic resonance spectra were measured prior to illumination and 1, 3, 7, 14, 21 and 28 days after PDT on each mouse. A drastic decrease in adenosine triphosphate (ATP) and a concomitant increase in inorganic phosphate (Pi) were evident on the first day after PDT in all cases. The beta-ATP/total phosphate (P) ratio was 0.64 +/- 0.29% (average +/- s.d.) in complete response, 0.67 +/- 0.30% in recurrence and 2.45 +/- 0.93% in partial response. Comparison of this ratio to the histological findings revealed that the beta-ATP/total P ratio reflects the HeLa cell tumours which survived PDT. In other words, partial response on the one hand was distinguished from complete response and recurrence on the other with this ratio 1 day after PDT (P < 0.05). In addition, the ratio of phosphomonoester (PME) to Pi rose beyond 1.0 when macroscopic recurrence occurred, while it stayed under 1.0 in complete response. This finding suggests that the recurrence of HeLa cell tumours can be detected by the PME/Pi ratio.

Adenosine Triphosphate↗

Short-chain acyl-CoA-dependent production of oxalate from oxaloacetate by Burkholderia glumae, a plant pathogen which causes grain rot and seedling rot of rice via the oxalate production.

In Burkholderia glumae (formerly named Pseudomonas glumae), isolated as the causal agent of grain rot and seedling rot of rice, oxalate was produced from oxaloacetate in the presence of short-chain acyl-CoA such as acetyl-CoA and propionyl-CoA. Upon purification, the enzyme responsible was separated into two fractions (tentatively named fractions II and III), both of which were required for the acyl-CoA-dependent production of oxalate. In conjugation with the oxalate production from oxaloacetate catalyzed by fractions II and III, acetyl-CoA used as the acyl-CoA substrate was consumed and equivalent amounts of CoASH and acetoacetate were formed. The isotope incorporation pattern indicated that the two carbon atoms of oxalate are both derived from oxaloacetate, and among the four carbon atoms of acetoacetate two are from oxaloacetate and two from acetyl-CoA. When the reaction was carried out with fraction II alone, a decrease in acetyl-CoA and an equivalent level of net utilization of oxaloacetate were observed without appreciable formation of CoASH, acetoacetate or oxalate. It appears that in the oxalate production from oxaloacetate and acetyl-CoA, fraction II catalyzes condensation of the two substrates to form an intermediate which is split into oxalate and acetoacetate by fraction III being accompanied by the release of CoASH.

Acetyl Coenzyme A↗

The role of chondroitin sulfate chains of urinary trypsin inhibitor in inhibition of LPS-induced increase of cytosolic free Ca2+ in HL60 cells and HUVEC cells.

Preincubation of HL60 cells and HUVEC cells with urinary trypsin inhibitor (UTI) inhibited increase of cytosolic free Ca2+ induced by LPS. In contrast, an increase of cytosolic free Ca2+ induced by LPS was not inhibited by deglycosylated UTI, UTI treated with monoclonal antibody of chondroitin sulfate. 45Ca2+ binding showed that UTI binds 45Ca2+ dose-dependently. Scatchard plot analysis showed that UTI has two binding sites for Ca2+, a high affinity binding site (Kd=15 microM) and a low affinity site (Kd=150 microM), and that UTI has more than 70 Ca2+ binding sites per molecule. The Ca2+ binding capacity of deglycosylated UTI and UTI treated with monoclonal antibody of chondroitin sulfate was markedly depressed. Furthermore, UTI forms multi-polymers in the presence of Ca2+ as demonstrated by gel filtration and agarose gel electrophoresis. These results suggest that UTI is a physiological Ca2+ chelator on the cells and that the action is due to chondroitin sulfate chains of UTI.

Binding Sites↗

The effects of sevoflurane on recovery of brain energy metabolism after cerebral ischemia in the rat: a comparison with isoflurane and halothane.

UNLABELLED: Isoflurane is an appropriate anesthetic for neuroanesthesia. We evaluated whether the effect of sevoflurane is similar to that of isoflurane or halothane on brain energy metabolism after cerebral ischemia followed by reperfusion using 31P-magnetic resonance spectroscopy. Wistar rats (n = 21) were divided into three groups: isoflurane-, sevoflurane-, or halothane-treated. After anesthesia induction and surgical preparation, each anesthetic concentration was adjusted to 1 minimum alveolar anesthetic concentration. Cerebral ischemia was induced with bilateral carotid occlusion and reduction of mean arterial blood pressure to 30-40 mm Hg by blood withdrawal. Magnetic resonance measurements were performed during ischemia and for 120 min of reperfusion. Intracellular pH in the isoflurane-treated, sevoflurane-treated, and halothane-treated groups decreased to 6.180 +/- 0.149, 6.125 +/- 0.134, and 6.027 +/- 0.157, respectively, at the end of ischemia. There were no differences in the change of phosphorous compounds and intracellular pH between the isoflurane-treated and the sevoflurane-treated groups during ischemia and reperfusion. However, in the halothane-treated group, we observed a significant delay in the recovery of adenosine triphosphate and intracellular pH (0.038 +/- 0.013 pH unit/min compared with 0.064 +/- 0.011 in the isoflurane-treated group and 0.058 +/- 0.008 in the sevoflurane-treated group) until 24 min of reperfusion (P < 0.05). We conclude that sevoflurane has effects similar to isoflurane on brain energy metabolism during and after cerebral ischemia. IMPLICATIONS: It is important to know whether anesthetics adversely effect brain metabolism during ischemia and reperfusion. A new anesthetic, sevoflurane, affected the brain in a manner similar to isoflurane, which has been used for many years as an anesthetic.

Adenosine Triphosphate↗

Effects of a prescription of Chinese herbal medicine on snake venom-induced nephropathy in mice.

A prescription of Chinese herbal medicine, tentatively named P-19, was examined for its inhibitory effect and its mechanism using an experimental model of nephropathy induced by purified snake venom proteinase, Ac(1)-proteinase (Ac(1)-P). The treated mice were injected with 0.1 ml of crude extract of P-19 intraperitoneally every other day beginning 2 d before to 1 week after the injection of Ac(1)-P. The non-treated mice were injected with saline instead of the medicine P-19. The physiological condition and histopathological observation of the mice at one week after Ac(1)-P injection were better in the treated group than in the non-treated group. This indicates that P-19 inhibited the production of glomerular lesions induced in mice by Ac(1)-P. The physiological condition and histopathological changes in the mice were better with P-19 treatment than with P-3 treatment. Differences in the mechanism of action between the crude extract of P-3 and P-19 are not only in diuretic action but also in the changes in the glomerular basement membrane. On the basis of spectrophotometric studies, phenolic carboxylates were confirmed to be contained in the crude extract of P-19, having a different chemical structure of caffeic acid, which is the effective component in P-3. Immunohistochemical observation revealed a difference between the groups. In the non-treated mice, deposits of the venom were clearly observed in the glomerular tuft and Bowman's capsule, corresponding to the histopathological changes, within 2.5 min after the injection of Ac(1)-P. In the treated mice, the deposits were indistinct in the Bowman's capsule. The difference was considered to be caused by changes in the glomerular basement membrane after P-19 treatment.

Agkistrodon↗

Creatine kinase kinetics in diabetic cardiomyopathy.

One feature of the diabetic cardiomyopathy is the appearance of contractile dysfunction as the workload increases. We hypothesized that this resulted from an impaired creatine kinase/phosphocreatine system and therefore examined the creatine kinase kinetics at both low and high workloads. Creatine kinase flux (by 31P nuclear magnetic resonance saturation transfer method), cardiac performance, and oxygen consumption were measured in control and streptozotocin-induced diabetic rat hearts. Creatine kinase flux was inhibited by iodoacetamide in control hearts to confirm the role of the creatine kinase/phosphocreatine system in cardiac performance. In diabetic hearts, 1) the contractile dysfunction became apparent only at high workloads, 2) the ATP synthesis rate was not significantly different from control hearts, 3) the creatine kinase flux was reduced by 30.8% (257.5 +/- 7.7 mumol.g wet wt-1.min-1 in control vs. 178.3 +/- 9.4 in diabetes, P < 0.001), and 4) the creatine kinase flux did not increase as the workload increased. In control hearts, 5) iodoacetamide inhibited the creatine kinase flux to the same degree as that in diabetic hearts, and 6) the contractile dysfunction was not as severe as that observed in diabetic hearts. These results suggest that the impaired creatine kinase/phosphocreatine system is, at least in part, responsible for the contractile dysfunction in the diabetic cardiomyopathy.

Adenosine Triphosphate↗

[Marked dilatation of the bilateral common carotid artery: a case report].

We reported a rare case of marked dilatation of the bilateral common carotid artery (CCA) associated with stenosis of the left middle cerebral artery (MCA). A 64-year-old female was admitted with right hemiparesis and dysarthria. She was hospitalized 2 years ago for cholecystitis. For 5 years, she has been under medical treatment for hypertension, diabetes mellitus, hyperlipidemia, cardiac failure associated with hypertrophic cardiomyopathy, and atrial fibrillation. Brain CT scan showed infarction of the left corona radiata. Angiography revealed marked dilatation of the bilateral CCA and the internal carotid artery (ICA), moderate dilatation of the innominate artery and the right subclavian artery, kinking of the right CCA, diverticular outpouching of the left ICA, and stenosis of the right external carotid artery and the left MCA. Breast CT scan revealed moderate dilatation and marked calcification of the ascending aorta and the aortic arch. Laboratory examination did not show any sign of inflammation, rheumatoid factor (RA), antistreptolysis-O (ASLO) and antinucleotic antibody. Based on the clinical course, radiological findings and laboratory data, possible diagnosis of the dilatation of the bilateral CCA was discussed with particular emphasis on arteriosclerotic aneurysm and aortitis syndrome.

Aortic Arch Syndromes↗

A hydrophilic tetrahydro-beta-carboline in human urine.

A substance that exhibited a tryptophan-like fluorescence peak at 354 nm on excitation at 295 nm at neutral pH was isolated from human urine. This compound was determined by visible-light absorption spectroscopy, fluorescence spectroscopy, 1H and 13C NMR spectroscopies, and FAB-MS to be 1-(1',2',3',4',5'-pentahydroxypentyl)-1,2,3,4-tetrahydro-2-carboli ne-3- carboxylic acid. This compound, named tetrahydropentoxyline, is a new type of hydrophilic tetrahydro-beta-carboline, and its elution position was between those of 4-pyridoxic acid and kynurenic acid on C18 reversed-phase HPLC. The amount of tetrahydropentoxyline excreted in the urine of normal subjects [n = 21; age, 45 (SD 20) years] was about 5.2 (SD 1.0) mg per day.

Carbolines↗

Analysis of selenium metabolites in urine samples of minke whale (Balaenoptera Acutorostrata) using ion exchange chromatography.

1. To study the distribution of selenium metabolites in whale urine, an analytical methodology for separation and determination has been developed. 2. From whale urine, five selenium components, including trimethylselenonium ion were separated and determined by a combination of ion exchange chromatography and fluorometry. 3. The mean urinary selenium level of five minke whales was 1500 ng/ml, with a standard deviation of 400 ng/ml, i.e., about 30 times as high as that for humans.

Animals↗

Effects of propranolol and diltiazem on the rate of high-energy phosphate metabolism in reperfused rat hearts--31P-NMR saturation transfer study.

The relationships between pressure rate product (PRP) and flux (PCr-->ATP) or flux (Pi-->ATP) were studied in isolated perfused rat hearts by the saturation transfer method using 31P-NMR. The effects of propranolol and diltiazem on phosphate metabolism were also studied. After a 40 min preischemic period, the hearts were subjected to a 15 min period of ischemia, followed by 60 min of reperfusion. Propranolol (0.4-1.2 microM) or diltiazem (3.0-6.0 microM) was infused for 30 min before ischemia and reinfused after reperfusion for 60 min. The flux (PCr-->ATP)/PRP ratio at reperfusion did not differ from that at preischemia. This value was also not affected by propranolol or diltiazem treatment. However, the flux (Pi-->ATP)/PRP ratio at reperfusion was significantly less than that at preischemia. Moreover, this value was significantly improved by propranolol or diltiazem treatment. This study demonstrates that 1) flux (PCr-->ATP) has a good correlation with cardiac performance, 2) stunned myocardium needs less ATP turnover for survival of its depressed contractile activity, and 3) flux (Pi-->ATP) can limit recovery of postischemic performance. Protective effects of propranolol and diltiazem are exerted on the flux (Pi-->ATP), i.e. ATP derived from glycolytic flux, in the reperfused heart.

Animals↗

Identification of effective component from a traditional herbal medicine and the inhibitory effects on experimental glomerular lesion in mice.

Effective constituents for renal disease were partially purified from a herbal prescription. The efficacy on renal diseases was examined using an experimental model system of glomerular lesion in mice induced by Agkistrodon acutus venom (Ac1-P). The extract of boiling water of the herbal prescription (P-3) was first fractionated by ether into an acidic fraction and a mixture of basic and neutral fractions. The acidic fraction was proved to be more effective and then further examined by thin layer chromatography and spectrophotometry. One of the main components was confirmed to be caffeic acid which had inhibitory effect on renal failure in mice by Ac1-P. This effect was considered to be caused by caffeic acid inhibiting the proteolytic enzyme activity of Ac1-P. Caffeic acid should thus have prophylactic or inhibitory effect on glomerular disease in which proteolytic enzymes may have pathogenic roles.

Animals↗

Bartter's syndrome with gouty arthritis.

A 45-year-old woman with Bartter's syndrome complicated with gouty arthritis is reported. Bartter's syndrome was diagnosed from hypokalemia, metabolic alkalosis, high plasma renin activity, normal blood pressure and attenuated pressor response to exogenous angiotensin II infusion. Serum uric acid was 11.8 mg/dl, the renal clearance of uric acid was low (3.0 ml/min) and fractional excretion of uric acid (FEUA) was 7.0%, being the lower limit of the normal range. Fractional excretion of phosphate was low (5.3%) and fractional free water clearance per fractional distal sodium delivery was 0.51. The mechanism of hyperuricemia in this case is discussed.

Arthritis, Gouty↗