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Biomedical subjects

S Shimizu

Publications and source records attributed to S Shimizu.

At least 559 records · Page 31Linked to original sources
PubMed1994

Enzyme release from mitochondria during reoxygenation of rat liver.

Reoxygenation-induced release of mitochondrial aspartate aminotransferase (mAST) into the cytosol was studied using perfused rat liver. As the absolute activity of mAST in the perfusate did not indicate the degree of mitochondrial enzyme release, the following 3 methods were applied: measurement of the mAST to total AST ratio in the efferent perfusate, the digitonin infusion method, and measurement of mAST activity in the cytosolic compartment isolated from perfused livers. The results by all 3 methods were consistent and showed that mitochondrial injury occurs on reoxygenation. The mitochondrial Ca2+ content was proportional to the extent of mAST release during reoxygenation, indicating involvement of Ca2+ in the enzyme release. CsA, a potent inhibitor of Ca(2+)-induced increase in permeability of the mitochondrial membrane, completely prevented mAST release on reoxygenation. We conclude that during reoxygenation of hypoxic liver, mAST leaks into the cytosol in a Ca(2+)-dependent, CsA-sensitive manner.

Animals↗
PubMed1994

Sweet's syndrome during therapy with granulocyte colony-stimulating factor in a patient with aplastic anaemia.

A patient with aplastic anaemia developed Sweet's syndrome (a febrile neutrophilic dermatosis) during granulocyte colony-stimulating factor (G-CSF) therapy. Three repeated episodes of appearance and disappearance of erythematous nodules after administration and withdrawal of G-CSF confirmed that G-CSF induced Sweet's syndrome in the patient. Sweet's syndrome has been reported in patients with myelodysplastic syndrome and acute leukemia, but not in patients with aplastic anaemia. This is the first report of a patient with aplastic anaemia who developed G-CSF-induced Sweet's syndrome.

Adult↗
PubMed1994

Reduction by NG-nitro-L-arginine of H2O2-induced endothelial cell injury.

1. The effects of three analogues of NG-nitro-L-arginine (L-NOARG) and NG-monomethyl-L-arginine (L-NMMA), inhibitors of nitric oxide (NO) synthase, on hydrogen peroxide (H2O2)-induced endothelial cell injury were studied. 2. Endothelial cell injury was assessed by measuring the release of intracellular lactate dehydrogenase (LDH) and 51Cr. 3. Addition of H2O2 (250-1,000 microM) to endothelial cells induced the release of LDH dose-dependently. The release of LDH was reduced by pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 10(-4)-4 x 10(-3) M), L-NOARG (10(-4)-4 x 10(-3) M) and NG-nitro-L-arginine benzyl ester (L-NABE, 10(-4)-4 x 10(-3) M), inhibitors of NO synthase. 4. L-NOARG analogues also reduced H2O2-induced 51Cr release from endothelial cells, while L-NMMA had no effect. 5. The protective effect of L-NAME was not reversed by addition of L-arginine (L-Arg, 1-10 mM). 6. Both L-NAME and L-NMMA completely inhibited L-Arg metabolism to L-citrulline coupled with NO synthesis. 7. These findings suggest that L-NOARG analogues but not L-NMMA reduced H2O2-induced endothelial cell injury, and that these effects may not be related to inhibition of NO production.

Amino Acid Oxidoreductases↗
PubMed1994

Erythropoietin response to acute hypobaric or anaemic hypoxia in gentamicin-administered rats.

In an attempt to assess the erythropoietin (Epo) production site(s) in rat kidney, Epo response to hypoxia and renal histopathological changes were studied in rats administered with graded doses of gentamicin. Male Sprague-Dawley rats of 9 to 11 weeks old were used. Following a 14-day subcutaneous administration (67.5 or 33.8 mg kg-1 day-1) of gentamicin, a nephrotoxic aminoglycoside, selective proximal tubular lesions were produced. These gentamicin-administered rats were compared with normal rats with respect to Epo response to hypoxia. Two different kinds of hypoxic load, either 0.35 atm hypobaric hypoxia (PIO2 = 46 torr) or acute anaemia (Ht: 29.3 +/- 0.2% and [Hb]: 9.7 +/- 0.3 g dl-1) by withdrawing of blood corresponding to 1-2% of body weight was used. During the hypoxic period of up to 48 h, the peak renal venous plasma Epo titres of 3.1 +/- 0.6 and 4.3 +/- 0.6 U ml-1 was observed at the 6th h in normal hypobaric hypoxic and anaemic rats, compared with the prehypoxic value of 0.7 +/- 0.1 U ml-1. The Epo titres then declined gradually. In the rats which were administered gentamicin, Epo response pattern was the same as that observed in the normal rats, but the peak value decreased significantly to 0.8 +/- 0.3 and 1.1 +/- 0.4 U ml-1 in hypoxic and anaemic rats (P < 0.05). Histological examination revealed the selective damage to renal proximal convoluted tubules. The Epo response was reduced by the tissue damages, and restoration of the gentamicin-induced tissue injury was accompanied with restored Epo response to hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia↗
PubMed1994

High affinity of blood for oxygen reduces oxygen uptake in contracting canine gracilis muscle.

To clarify the influence of blood flow with high-oxygen (O2)-affinity blood on oxygen consumption (VO2) in submaximally exercising skeletal muscle, we perfused the isolated dog gracilis (n = 8) contracting under 1 Hz stimulation alternatively with normal and high-O2-affinity blood, with a constant arterial O2 content (Ca,O2) and varying perfusion rates. The average P50 (oxygen partial pressure (PO2) for half-saturation at pH 7.40, PCO2 of 40 mmHg at 37 degrees C) of the high-O2-affinity blood prepared by carbamylation was 15.5 mmHg, and that of the normal blood 33.7 mmHg. With normal blood perfusion, the average VO2 above 6 ml min-1 (100 g)-1 of O2 delivery (Ca,O2 x flow) was 4.38 ml min-1 (100 g)-1 (range 4.17-4.68 ml min-1 (100 g)-1, and VO2 at the O2 delivery range of 6-5 and 4-2.5 ml min-1 (100 g)-1 decreased to 3.96 and 2.43 ml min-1 (100 g)-1, respectively. The PO2 of venous effluent (Pv,O2) at the O2 delivery of 6 ml min-1 (100 g)-1 was 33 mmHg. With low-P50 blood perfusion, VO2 was significantly less than with normal blood, both below the O2 delivery level of 6 ml min-1 (100 g)-1 and above it, even in the fairly high O2 delivery range of 8.5-12 ml min-1 (100 g)-1 (P < 0.05). Thus, high blood flow did not compensate for the reduced VO2 caused by high-O2-affinity blood. At values of Pv,O2 less than 33 mmHg, VO2 with low-P50 blood was not significantly different from that with normal blood (P > 0.05). The reduced VO2 in submaximally exercising skeletal muscle might be due to a slower O2 dissociation from the high-O2-affinity red cells and to a limited O2 diffusion resulting from the lower Pv,O2 value (which reflects mean end-capillary PO2).

Animals↗
PubMed1994

Effects of recombinant superoxide dismutase on manganese superoxide dismutase gene expression in gerbil hippocampus after ischemia.

BACKGROUND AND PURPOSE: We reported that recombinant human superoxide dismutase ameliorates delayed neuronal death in the postischemic gerbil hippocampus. Since postischemic induction of copper-zinc superoxide dismutase messenger RNA was abolished by this treatment, oxygen radicals generated on reperfusion may induce the expression of this gene. In the present study we examined whether oxygen radicals also induce the expression of manganese superoxide dismutase messenger RNA in the postischemic brain. METHODS: We induced transient cerebral ischemia by occluding the bilateral common carotid arteries of gerbils. Recombinant human superoxide dismutase (8 x 10(5) U/kg) or apo-superoxide dismutase was administered intravenously 1 minute before a 5-minute occlusion of the carotid arteries. We analyzed both copper-zinc and manganese superoxide dismutase RNA by in situ hybridization histochemistry and by Northern and dot blot analyses using radioisotope-labeled oligonucleotide probes. RESULTS: Hybridization with the manganese superoxide dismutase messenger RNA occurred at the limit of detection in normal CA1 neurons. We observed striking increases in the labeling of CA1 up to 24 hours after 5 minutes of ischemia. The hybridization occurred anew in glial cells of the CA1 layer during 3 to 7 days. Pretreatment with recombinant human superoxide dismutase had no effect on the postischemic induction of manganese superoxide dismutase messenger RNA, whereas the same treatment significantly attenuated (P < .01) the increase in copper-zinc superoxide dismutase messenger RNA. CONCLUSIONS: Our results demonstrated temporal postischemic induction of manganese superoxide dismutase messenger RNA. The inducer may not be superoxide radicals but may be other chemical mediators such as cytokines.

Amino Acid Sequence↗
PubMed1994

Risk factors for carotid atherosclerosis and platelet activation.

Thromboxane A2 biosynthesis was studied in healthy subjects, in patients in whom the extent of carotid atherosclerosis was determined, and in patients receiving chronic aspirin treatment, to determine what factors activate platelets to develop carotid atherosclerosis. Urinary 11-dehydrothromboxane B2, a major metabolite of thromboxane A2, was measured by radioimmunoassay after purification by reverse-phase HPLC. The extent of carotid atherosclerosis was determined by real-time B-mode ultrasonography. The severity of carotid atherosclerosis in each subject was evaluated by plaque score, which was computed by summing the maximum thickness of plaque measured in millimeters. Urinary excretion of 11-dehydrothromboxane B2 in healthy subjects was higher (P < 0.01) in cigarette smokers (1063 +/- 244 ng/g creatinine) than in non-smokers (815 +/- 183 ng/g creatinine). Aspirin significantly suppressed 11-dehydrothromboxane B2 excretion (266 +/- 114 ng/g creatinine). In the 24 patients in whom the plaque score was measured, multivariate analysis indicated a significant positive correlation between urinary excretion of 11-dehydrothromboxane B2 and plaque score, age, smoking and hypercholesteremia. Our results indicate that risk factors such as age, hypercholesteremia, atherosclerosis and smoking activate platelets in vivo to develop carotid atherosclerosis.

Adult↗
PubMed1994

Elevated cytokine levels in synovial fluid of rheumatoid arthritis correlates with the presence of cytomegalovirus genome.

Synovial fluid aspirated from 34 patients with symptomatic rheumatoid arthritis (RA) was evaluated for the presence of human cytomegalovirus (CMV) genomic material using polymerase chain reaction (PCR), and for levels of interleukin 8 (IL-8) and IL-6 using enzyme-linked immunoadsorbence assay. IL-8 and IL-6 levels were significantly higher in CMV DNA-positive RA patients than CMV DNA-negative RA patients and at least 10-fold higher than in both corresponding control groups of patients with osteoarthritis (OA). These findings suggest an association between elevated IL-8 and IL-6 levels and the presence of the CMV genome in RA patients.

Arthritis, Rheumatoid↗
PubMed1994

[Transitional cell carcinoma of bladder occurring during pregnancy: report of two patients].

Primary transitional cell carcinoma (TCC) of the bladder occurring during pregnancy is extremely rare and only 16 patients have been reported in the literature. Patient 1: A 24-year-old primigravida at 33 weeks of gestation presented with gross hematuria. Cystoscopy revealed a large bladder tumor. After delivery TUR-Bt was performed. Because of frequent reccurrences after TUR-Bt, radical cystectomy was done. Pathological study revealed transitional cell carcinoma, G1-G2, pTa. Patient 2: A 34-year-old gravida 11 at 6 weeks of gestation presented with gross hematuria. Cystoscopy revealed a papillary bladder tumor. TUR-Bt was performed after artificial abortion. Pathological study revealed papillary transitional cell carcinoma, G1 > G2, pTa. Eighteen patients of TCC of the bladder occurring during pregnancy were reviewed. Fifteen of the 18 patients presented with gross hematuria. All patients had superficial, solitary, grade 1 or 2 papillary TCC, except one grade 3 patient. Cystoscopy should be considered in all pregnant women with gross hematuria. Small TCCs of the bladder during pregnancy can be treated safely by TUR-Bt during pregnancy or after delivery.

Adult↗
PubMed1994

Bradykinin induces generation of reactive oxygen species in bovine aortic endothelial cells.

We investigated the effects of bradykinin on intracellular oxidative stress in bovine aortic endothelial cells using a hydroperoxide-sensitive fluorescent dye, 2',7'-dichlorofluorescein (DCFH), and a laser scanning confocal microscope. Bradykinin induced an immediate increase in intracellular Ca2+ concentration, and stimulated the oxidation of DCFH in cultured endothelial cells. This bradykinin-induced oxidation of DCFH was inhibited by pretreatment with N-(2-mercaptopropionyl)-glycine (MPG) and 1,3-dimethyl-thiourea (DMTU), scavengers of hydroxyl radical, and the removal of extracellular Ca2+ but was unaffected by NG-nitro-L-arginine or NG-monomethyl-L-arginine, both inhibitors of nitric oxide (NO) synthase. On the other hand, pretreatment with indomethacin and aspirin, inhibitors of cyclooxygenase, inhibited bradykinin-induced oxidation of DCFH. These findings suggest that bradykinin increases intracellular Ca2+ and stimulates the generation of hydroxyl radical-like reactive oxygen species (scavenged by MPG or DMTU) via the cyclooxygenase pathway but not via the reaction of NO and superoxide anion.

Amino Acid Oxidoreductases↗
PubMed1994

Stimulation by hydrogen peroxide of L-arginine metabolism to L-citrulline coupled with nitric oxide synthesis in cultured endothelial cells.

The effect of hydrogen peroxide on metabolism of L-arginine to L-citrulline in the biosynthesis of nitric oxide was investigated in bovine aortic endothelial cells. Addition of hydrogen peroxide (1-10 mM) to endothelial cells increased L-citrulline formation from L-arginine in a dose-dependent manner. Stimulation of L-citrulline formation was prevented by catalase (20 micrograms/ml), a hydrogen peroxide scavenger, but not by superoxide dismutase (SOD, 100 micrograms/ml), a superoxide anion scavenger. Pretreatment with NG-nitro-L-arginine (10(-5) M) and NG-methyl-L-arginine (10(-4) M), potent inhibitors of nitric oxide synthase, also inhibited L-citrulline formation induced by hydrogen peroxide. Moreover, hydrogen peroxide increased intracellular Ca2+ concentrations, and the removal of extracellular Ca2+ reduced the hydrogen peroxide-induced formation of L-citrulline. These findings show that hydrogen peroxide increases the intracellular Ca2+ concentration and stimulates the formation of L-citrulline from L-arginine coupled with nitric oxide synthesis in cultured endothelial cells.

Animals↗
PubMed1994

[Phase I clinical study for 111In-DTPA-IgG].

A phase I study was performed in three health volunteers to evaluate the safety and biodistribution of 111In-DTPA-IgG, a newly developed imaging agent for inflammation/infection. No adverse effect was observed. There were no clinically significant changes in blood chemistry, hematology, and urinalysis parameters, physical examinations or vital signs. 111In-DTPA-IgG in blood exhibited a biexponential disappearance, consisting of a fast component (t1/2 alpha) ranging from 5.72 to 8.51 hours, and a slow component (t1/2 beta) ranging from 34.0 to 35.5 hours. Twelve percent of the injected dose was eliminated in the urine within 72 hours. Dosimetry estimates indicated that up to 80 MBq of 111In-DTPA-IgG can be safely administered to subjects without exceeding generally accepted absorbed dose for other scintigraphic procedures for inflammation/infection. The organs receiving the highest absorbed dose was the liver followed by the kidneys, heart, and lungs. Each of these organs received less than 40 mGy per 80 MBq administered. The safety data and dosimetry estimates indicated that it is safe to proceed with phase II studies with a 40-80 MBq dose of 111In-DTPA-IgG.

Adult↗
PubMed1994

[A technique of successfully performing an annuloplasty for narrowed aortic valvular annulus in aortic valve replacement].

We previously reported that a significant reduction in both myocardial weight and left ventricular end-diastolic volume weight and left ventricular end-diastolic volume was achieved with the use of an artificial valve of 21 mm size in aortic valve replacement (AVR) performed on aortic stenosis patients with a body surface area of less than 1.4 m2. In those patients with a narrower valvular annulus on a unit body surface area basis, however, we have aggressively performed an operation of enlarging the valvular annulus in conjunction with AVR with a similar satisfactory hemodynamic improvement invariably in all cases, including 3 without autologous blood transfusion. In this paper mention is made, based on our experiences gained so far, of some points of critical technical importance for the successful performance of AVR involving annuloplasty, specification by the Manouguian's and Konno's procedure.

Adolescent↗
PubMed1994

[Two cases of pericardial rupture due to blunt chest trauma].

We treated two cases of pericardial rupture from blunt chest trauma. Case 1: A 55-year-old male was injured in an automobile accident. He recovered from the left hemothorax by tube drainage. One year and two months after the trauma, a left pericardial rupture was found during an operation for a left diaphragmatic hernia. As the epicardium adhered firmly to the pericardium, the ruptured pericardium was not sutured. Case 2: A 46-year-old man fell from a tree five meters in height. Chest radiography showed multiple right rib fractures, a pelvic fracture, pneumopericardium, and right hemopneumothorax. After four days, we performed a thoracoscopic examination under local anesthesia. The thoracoscopy revealed a rupture as large as an egg in the right pericardium anterior to the phrenic nerve. Judging from the size of the rupture, cardiac luxation was suspected not to have occurred. So the defect was not repaired. These two patients were discharged uneventfully without cardiac luxation. In the future, the accumulation of thoracoscopic findings may provide adequate information for judging the indication of operative repair in pericardial ruptures.

Humans↗
PubMed1994

[Parvovirus B19-induced aplastic crisis in a patient with iron deficiency anemia].

A 38-year-old female was referred to Takaoka City Hospital for treatment of common-cold-like symptom and an episode of transient unconsciousness. Physical examination on admission revealed severe anemia and an ejection heart murmur. Complete blood count revealed microcytic hypochromic anemia (Hb 4.1 g/dl), leukocytopenia (2.600/microliters), thrombocytopenia (7.1 x 10(4)/microliters) and reticulocytopenia (17,000/microliters). The bone marrow cellularity was within normal limits. Cells in the erythroid series were decreased to 5% of total bone marrow nucleated cells with maturation arrest at the level of proerythroblasts. Giant proerythroblasts were observed in 0.2% of marrow nucleated cells. No stainable iron was seen. Both anti-parvovirus B19 IgM antibody and IgG antibody were positive in the serum and parvovirus B19 DNA was detected in the bone marrow cells by polymerase chain reaction. From these results, iron deficiency anemia complicated with pure red cell aplasia secondary to parvovirus B19-induced infection was diagnosed. The anemia gradually improved with administration of sodium ferrous citrate one month after admission. Parvovirus B19 has been reported to cause an aplastic crisis in the patients who has a rapid red cell turn over such as hemolytic anemia or acute blood loss. This report suggested that severe aplastic crisis is also induced in patients with iron deficiency anemia by parvovirus B19-induced infection and warns that careful observation is necessary for the follow up of patients with iron deficiency anemia.

Adult↗