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Biomedical subjects

Y Yazaki

Publications and source records attributed to Y Yazaki.

854 records · Page 48Linked to original sources
PubMedDate not supplied

Effects of intravenous disopyramide on coronary hemodynamics and vasodilator reserve in hypertrophic obstructive cardiomyopathy.

Disopyramide reduces the subaortic pressure gradients and improves the clinical symptoms of patients with hypertrophic obstructive cardiomyopathy. Changes in coronary hemodynamics and vasodilator reserve in response to this agent have not been evaluated in such patients. To assess the acute effects of intravenous administration of disopyramide on coronary hemodynamics, microvascular dilatory capacity, and balance between myocardial oxygen supply and demand in hypertrophic obstructive cardiomyopathy, we examined 12 patients using an intravascular Doppler catheter and spectral analysis. Intravenous disopyramide 100 mg over 10 min caused mild increases in heart rate and aortic systolic pressure and a significant fall in left ventricular systolic pressure, resulting in a 13% decrease in the product of heart rate and left ventricular systolic pressure (from 1.13 +/- 0.18 x 10(4) before disopyramide to 0.98 +/- 0.17 x 10(4) beats/min x mm Hg 10 min afterwards; p < 0.05) and a reduction in the resting peak systolic pressure gradients of the left ventricular outflow tract. There was a 14% reduction in coronary blood flow (from 93.5 +/- 13.2 to 80.3 +/- 11.6 ml/min; p < 0.05) with an increase in coronary resistance (from 0.94 +/- 0.16 to 1.23 +/- 0.21 mm Hg/ml/min; p < 0.001). The index of coronary vasodilator reserve remained unchanged. These findings suggest that intravenous disopyramide causes a coronary vasoconstrictive effect without significantly changing the coronary microvascular dilatory capacity, but this effect may not be harmful to the balance between myocardial oxygen supply and demand in patients with hypertrophic obstructive cardiomyopathy.

Adult↗
PubMedDate not supplied

Presence of contractile-type smooth muscle cells in the endocardium.

A smooth muscle layer exists in the parietal endocardium. Notwithstanding previous pioneer work, little has been known on the phenotypes of these smooth muscles. In humans as in animals, smooth muscles show two distinct phenotypes, the 'synthetic' and 'contractile' states, which can be differentiated on the basis of the expression of two types of myosin heavy chain isoforms, SM1 and SM2. In this study, using SM1- and SM2-specific monoclonal antibodies, we performed immunohistochemical examinations to determine the phenotype of the endocardial smooth muscles. We report here that the endocardial smooth muscles have the contractile phenotype.

Antibodies, Monoclonal↗
PubMedDate not supplied

Overexpression of low density lipoprotein receptor on Chinese hamster ovary cells generates foam cells.

The atherosclerotic lesion is characterized by the presence of cholesterol-loaded foam cells. Chinese hamster ovary (CHO) cells do not normally store cholesteryl esters because low density lipoprotein (LDL) receptors are suppressed by exposure of these cells to LDL cholesterol. We transfected LDL receptor cDNA linked to the simian virus 40 early promoter into CHO cells (CHO 29) and found that LDL receptor binding in these cells was not suppressed by an excess amount of LDL cholesterol, indicating no regulation of the LDL receptor in CHO 29 cells. Furthermore, CHO 29 cells showed a high activity of LDL uptake and intracellular accumulation of cholesteryl esters. Light-microscopic examination demonstrated the resulting formation of foam cells in CHO 29 cells in the presence of 5 micrograms LDL/ml. These results demonstrated that foam cell changes in atherosclerotic lesions can be reproduced in CHO cells, whose LDL receptor activity is overexpressed, through the mechanism of LDL receptor-mediated endocytosis of native LDL.

Animals↗
PubMedDate not supplied

Effects of human recombinant macrophage colony-stimulating factor on the secretion of lipoprotein lipase from macrophages.

The effects of human recombinant macrophage colony-stimulating factor (M-CSF) on the secretion of lipoprotein lipase were studied in rat alveolar macrophages. Five nanograms per milliliter M-CSF significantly enhanced lipoprotein lipase secretion (threefold), and the maximal effect (10-fold) of M-CSF on lipoprotein lipase secretion was observed at a dose of 200 ng/ml M-CSF. The effect of M-CSF was time dependent but was not manifested during the first 8 hours of incubation. After 24 hours, its effects were evident and dose dependent. On blot hybridization of macrophage RNAs with human cDNA of lipoprotein lipase, a remarkable and dose-dependent increase in mRNA level (7.3-fold) was found in M-CSF-treated alveolar macrophages. The secretion of lipoprotein lipase was also enhanced in human monocyte-derived macrophages (2.6-fold), whereas the secretion from either THP-1 cells, P388 cells, or J774 cells was not significantly enhanced. These results indicate that the stimulation of lipoprotein lipase secretion after M-CSF treatment was evident in rat alveolar macrophages and human monocyte-derived macrophages on the basis of both enzyme activity and mRNA level; therefore, M-CSF may be involved in lipoprotein metabolism of macrophages through modulation of the secretion of lipoprotein lipase.

Animals↗
PubMedDate not supplied

Treatment of infective endocarditis with granulocyte colony-stimulating factor.

Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein hormone which stimulates the proliferation and differentiation of a subset of granulocyte precursors and enhances some functional activities of mature neutrophils. We tested the effects of G-CSF on a patient with intractable infective endocarditis. The white blood cell count was increased 3-fold and the inflammatory reactions such as C-reactive protein and erythrocyte sedimentation rate were completely normalized without any side effects. This is the first report describing the use of G-CSF for infective endocarditis. Administration of G-CSF might be suitable for treating intractable infections which cannot be controlled by antibiotics alone.

Aged↗
PubMedDate not supplied

Immunohistochemical localization of bone morphogenetic proteins and the receptors in epiphyseal growth plate.

The expression of bone morphogenetic proteins (BMPs) and BMP receptors (BMPRs) in the epiphyseal growth plate has not been clarified. In this study, we studied immunohistochemically the spatial and temporal localization of BMP-2/4, osteogenic protein-1 (OP-1, or BMP-7), and BMP receptors (BMPR-IA, BMPR-IB, and BMPR-II) in the epiphyseal plate of growing rats. The proximal parts of tibia in growing rats were observed. At 12 weeks after birth, BMP-2/4 and OP-1 were expressed markedly in proliferating and maturing chondrocytes. BMPR-IA, IB and II were clearly co-expressed in proliferating and maturing chondrocytes, and the expression was decreased in hypertrophic chondrocytes. At 24 weeks, the expression of BMP-2/4 and OP-1 was decreased, but BMPRs were still well-expressed in proliferating chondrocytes. The temporal and spatial expression of BMP and BMPR suggests that BMP and BMP receptors play roles in the multistep cascade of enchondral ossification in the epiphyseal growth plate.

Aging↗