[Right ventricular volume characteristics in postreparative patients with tetralogy of Fallot or transposition of the great arteries (author's transl)].
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Biomedical subjects
Publications and source records attributed to S Kitamura.
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Case histories are reported of three patients, 1 to 4 years of age, with severe mitral regurgitation that occurred as a sequela of mucocutaneous lymph node syndrome (MCLS). These patients were found among 12 patients with coronary artery lesions such as aneurysms, narrowings, and obstructions. One of them with multiple coronary aneurysms and also severely impaired left ventricular function died of congestive heart failure in the 2 years and 7 months' follow-up period after the acute illness. The second patient, 1 year of age, had multiple coronary aneurysms and mitral regurgitation. Because of the difficulty in treating coronary artery lesions at this patient's age and also because of medically controllable mitral regurgitation at present, this patient is now under careful observation. The third patient, whose condition was complicated by inferior wall myocardial infarction due to occlusion of the right coronary artery, underwent mitral valve replacement for intractable heart failure and cardiac cachexia. This patient had slow but definite improvement postoperatively. Mitral regurgitation secondary to MCLS usually is complicated by the associated difficult coronary artery lesions and impaired left ventricular function. Although this fact causes an extra-difficult situation, mitral regurgitation consequent to MCLS is amenable to surgical treatment and this disease should now be considered as a new surgical entity.
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A study was carried out in 40 patients with bronchial asthma to assess the therapeutic effect of co-dergocrine ('Hydergine'), an alpha-adrenergic receptor blocking agent, when added to their standard treatment with a beta-adrenergic receptor stimulant and aminophylline. Co-dergocrine administration (3 to 6 mg per day) brought about marked improvement in 25% and an improvement in 55% of the patients. The results suggest that co-dergocrine could be a useful drug when combined with other bronchodilators in the treatment of bronchial asthma.
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Xanthine oxidase (xanthine:oxygen oxidoreductase, EC 1.2.3.2) supplemented with an electron donor could catalyze the cis-trans isomerization of 3-(5-nitro-2-furyl)-2-(2-furyl)acrylamide, 3-(5-nitro-2-furyl)-2-phenylacrylamide and 3-(5-nitro-2-furyl)-2-(2-furyl)acrylonitrile. The direction of isomerization (cis leads to trans, cis in equilibrium trans or trans leads to cis) is dependent on the chemical structure of these nitrofuran derivatives. Lipoyl dehydrogenase (NADH:lipoamide oxidereductase, EC 1.6.4.3), DT-diaphorase (NAD(P)H:(quinone-acceptor) oxidoreductase, EC 1.6.99.2) and liver microsomes could also catalyze the conversion of cis-3-(5-nitro-2-furyl)-2-(2-furyl)acrylamide to its trans isomer in the presence of an appropriate electron donor. Such isomerizing activity of these enzymes is much higher than their nitro-reducing activity. In addition, the cis-trans isomerization of some nitrofuran derivatives was demonstrated with the liver slices and the small intestines of rats. A new cis-trans isomerization mechanism which is based on transfer of a single electron by an enzyme system to a nitrofuran derivative to give the radical-anion was proposed. This postulated mechanism was supported by the preliminary experiments using pulse radiolysis technique.
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An unusual anomaly of a solitary kidney with a solitary calix in siblings is described.
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Funtional characteristics of the single ventricle were studied by means of biplane angiocardiography in 34 patients. Group 1 consisted of 14 patients with normal or increased pulmonary vascular marking on chest film and no pulmonary stenosis. Group 2 included 20 patients with severe angiographic pulmonary stenosis and decreased pulmonary vascular marking. Ventricular volume parameters were calculated according to Simpson's rule and were compared with normal values. The sum of the normal left and right ventricular volumes was assumed to be 100%. In group 1, ventricular end-diastolic volumes averaged 143 +/- 11% and were significantly (p less than 0.001) larger than end-diastolic volumes in group 2 (81 +/- 4%). The presence or absence of severe pulmonary stenosis affecting pulmonary blood flow was a main factor regulating the ventricular chamber size in single ventricle. In both groups, the ejection fraction of a single ventricle was significantly lower than that of a normal left or right ventricle. Ventricular size and function in patients with a single ventricle should be carefully assessed before ventricular septation surgery.
Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.
Radioimmunoassay of 5alpha, 7alpha-dihydroxy-11-keto-tetra-norprosta-1,16-dioic acid, main urinary metabolite of prostaglandin F2alpha (PGF2alpha-MUM), was performed in patients with various respiratory diseases including diffuse interstitial fibrosing pneumonitis (DIFP, fibrosing alveolitis). Twenty-four hr excretion of PGF2alpha-MUM in patients with primary lung cancer, pulmonary fibrosis secondary to collagen diseases and stationary DIFP was normal. On the other hand, 24 hr excretion of PGF2alpha-MUM in patients with carcinomatous pleuritis was high and that in patients with aggravating DIFP was markedly high. There was no correlation between serum LDH levels and 24 hr excretion of PGF2alpha-MUM.
The effects of tartrazine on the synthesis of prostaglandin-like substances (PGLS) from arachidonic acid in isolated perfused guinea pig lung, and on the contractile responses of guinea pig tracheal tissues induced by histamine, acetylcholine, bradykinin, serotonin and prostaglandin F2 alpha were studied. The synthesis of PGLS from arachidonic acid was not inhibited by tartrazine. The contractile responses of guinea pig tracheal tissues induced by various bronchoconstrictors were potentiated in the presence of tartrazine. These results may suggest that tartrazine-induced asthma is not induced by inhibition of PGLS synthesis, but induced by potentiation of bronchoconstrictor responses.
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