[Application of fibrin glue in cardiovascular surgery].
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Biomedical subjects
Publications and source records attributed to S Kitamura.
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NAD (P) H-dependent reduction of nicotinamide N-oxide was investigated with rabbit liver preparations. Microsomes, microsomal NADPH-cytochrome c reductase or cytosolic aldehyde oxidase alone exhibited no nicotinamide N-oxide reductase activity in the presence of NADPH or NADH. However, when the microsomal preparations were combined with the cytosolic enzyme, a significant N-oxide reductase activity was observed in the presence of the reduced pyridine nucleotide. The activity was enhanced by FAD or methyl viologen. Cytosol alone supplemented with NADPH or NADH exhibited only a slight, but when combined with microsomes, a significant N-oxide reductase activity. Based on these facts, we propose a new electron transfer system consisting of NADPH-cytochrome c reductase and aldehyde oxidase, which exhibits nicotinamide N-oxide reductase activity in the presence of the reduced pyridine nucleotide.
Reduction of tertiary amine N-oxides to the corresponding amines by liver preparations was investigated with imipramine N-oxide and cyclobenzaprine N-oxide under anaerobic conditions. Rabbit liver cytosol in the presence of an electron donor of aldehyde oxidase exhibited a significant N-oxide reductase activity which is comparable to the activity of the liver microsomes supplemented with NADPH. Rabbit liver aldehyde oxidase also exhibited the N-oxide reductase activity in the presence of its electron donor, indicating that the activity observed in the liver cytosol is due to this cytosolic enzyme. Furthermore, the tertiary amine N-oxide reductase activity of liver cytosols from rats, mice, hamsters and hogs was demonstrated by comparison with that of liver microsomes from these mammalian species.
The present paper describes that mammalian liver aldehyde oxidase is involved in the reduction of nicotinamide N-oxide to nicotinamide. Rabbit liver aldehyde oxidase supplemented with its electron donor exhibited a significant nicotinamide N-oxide reductase activity under anaerobic conditions. Liver cytosols from rabbits, hogs, guinea pigs, hamsters, rats and mice, all of them, similarly exhibited the N-oxide reductase activity in the presence of an electron donor of aldehyde oxidase, but not xanthine oxidase. The cytosolic N-oxide reductase activity was almost completely inhibited by menadione, an inhibitor of aldehyde oxidase.
The present study provides the first evidence for in vitro metabolic conversion of a 1,1-disubstituted hydrazine to the corresponding nitrosamine. The study shows that superoxide radical which is generated by NADPH-cytochrome c reductase is involved in the oxidation of 1,1-diphenylhydrazine to N-nitrosodiphenylamine catalyzed by rat liver microsomes.
We measured plasma cortisol levels during surgery in seven neonates within ten days after birth and in 14 infants ranging in age from three months to 11 months. The 14 infants were divided into two groups; Group I included eight infants in whom general anaesthesia was maintained with oxygen, nitrous oxide and a muscle relaxant, Group II, six infants in whom general anaesthesia was maintained with oxygen, nitrous oxide, halothane and a muscle relaxant. In the neonates, the changes in mean plasma cortisol levels during anaesthesia were not statistically significant. In both Group I and Group II infants, the mean cortisol levels gradually rose during anaesthesia, but the initial rise in plasma cortisol levels was suppressed in the patients who received halothane.
The in vivo metabolism of an antibacterial nitrofuran, furazolidone [N-(5-nitro-2-furfurylidene)-3-amino-2-oxazolidone] was investigated. When the nitrofuran was administered orally to rats, two new-type nitrofuran metabolites, N-(4-carboxy-2-oxobutylideneamino)-2-oxazolidone and alpha-ketoglutaric acid, were isolated from the urine, together with 3-(4-cyano-2-oxobutylideneamino)-2-oxazolidone and N-(5-acetamido-2-furfurylidene)-3-amino-2-oxazolidone. In addition, the present study showed that the corresponding aminofuran was an intermediate in the conversion of furazolidone to these metabolites.
We investigated the effect of the thromboxane synthetase inhibitors, OKY-046 and OKY-1580, on the action of bronchoactive agents in guinea pig tracheal strips, and on arachidonic acid metabolism in isolated perfused guinea pig lung lobes. OKY-046 and OKY-1580 attenuated histamine-, serotonin-, acetylcholine-, bradykinin- and prostaglandin F2- induced contractile responses in guinea pig tracheal strips dose-dependently and potentiated isoproterenol-, salbutamol- and prostaglandin E2-induced relaxation in guinea pig tracheal strips dose-dependently. In addition, OKY-046 and OKY-1580 inhibited the biosynthesis of thromboxane A2 and accelerated the production of 6-keto prostaglandin F1 from arachidonic acid in isolated perfused guinea pig lung lobes. The above results suggest that OKY-046 and OKY-1580 might be useful therapeutic agents for the treatment of pulmonary thromboembolism and chronic obstructive lung diseases.
A new method of closing a perimembranous malalignment ventricular septal defect (VSD) in corrected transposition of the great arteries (TGA) of the [S,L,L] type is presented. The method consists of combined approaches to the VSD through both a right atriotomy and an aortotomy without a ventriculotomy. The VSD is patched obliquely from the morphological right ventricular side of the septum, cranially through the aortic valve to the left ventricular side of the septum, caudally through the mitral valve. Although this method has been successfully applied in only one adult patient, some advantages may be expected: (1) prevention of trauma to the His bundle, which runs along the anterosuperior rim of the VSD on the left ventricular side; and (2) prevention of trauma to the tricuspid, mitral, and aortic valves without having to open the ventricles. We believe that this new method warrants a further trial as possibly better for closure of the VSD in corrected TGA of the [S,L,L] type.
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1-Nitropyrene and nitrofurazone reductases in Escherichia coli B/r were studied comparatively. Nitrofurazone reductase activity was oxygen-insensitive, whereas 1-nitropyrene reductase activity was markedly inhibited by oxygen in both intact cells and cell-free preparations. The former activity depended upon reduced nicotinamide adenine dinucleotide or reduced nicotinamide adenine dinucleotide phosphate, whereas the latter activity upon flavin-adenine dinucleotide (FAD) as well as the reduced pyridine nucleotide. E. coli B/r acquired resistance to nitrofurazone in two mutational steps, associated with stepwise loss of the oxygen-insensitive nitrofuran reductase activity. However, 1-nitropyrene reductases were not affected at all by the mutation. These facts indicated that the major enzymes responsible for the reduction of 1-nitropyrene and nitrofurazone in E. coli B/r were different from each other. 1-Nitropyrene reductases were resolved by diethylaminoethyl-cellulose column chromatography into four enzymes all of which seem to reduce FAD, too. Among them, three enzymes appear to be able also to catalyze the reduction of nitrofurazone under anaerobic conditions.
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Pre- and postoperative hemodynamics were assessed in 14 consecutive patients who developed ventricular septal perforation (VSP) following acute myocardial infarction (AMI). Results were correlated with the surgical outcome and with postoperative clinical improvements. The patients were divided into 3 groups according to the time intervals between the onset of AMI and the operation; acute (within 2 weeks after AMI), subacute (between 2 and 4 weeks) and chronic (after 4 weeks). In the above groups, 6, 2 and 6 patients were included, respectively. Eleven patients had anteroseptal infarction and 3 patients sustained inferior infarction. The survival rates were 33, 50 and 100% in the acute, subacute and chronic groups, respectively with an overall survival rate of 64%. Hemodynamic comparisons between survivors and non-survivors revealed that the systolic aortic pressure and left ventricular stroke volume index were significantly higher and the right ventricular end-diastolic pressure was significantly lower in survivors than in non-survivors (p less than 0.05). Although no statistical significance was obtained, left ventricular end-diastolic volumes and ejection fractions were higher in survivors. No difference was present between survivors and non-survivors in either Qp/Qs, Pp/Ps, Rp/Rs, systolic pulmonary pressure, left ventricular end-diastolic pressure or cardiac index. Patients with low arterial pressure and high right ventricular end-diastolic pressure under intensive medical regimens, indicating the presence of cardiogenic shock and/or associated right ventricular infarction or severe failure, had a high mortality and should be considered for emergency operation. Postoperative hemodynamics improved significantly in all variables measured (p less than 0.05-0.01). Patients with a VSP should all be considered for surgery unless a definite contraindication exists.
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