Biomedical subjects
Publications and source records attributed to S Sagawa.
An automatic watering device was developed for the pika (Ochotona rufuescens rufescens), using drinking nozzles for rat and plastic pipes. This device was used for at least one year without any mechanical troubles, resulting in labor saving of animal caretakers. No difference in growth was observed between pikas reared with the automatic watering device and those maintained with conventional watering bottles.
Methods to quantitate changes in plasma volume based on changes in the hematocrit, which have been widely used in human subjects and large animals, were tested in small animals, such as rats. A modified equation was derived for application of the hematocrit method to small animals.
The relation of membrane lipids and osmotic fragility of red cells of human and rat were studied in vitro by repletion and depletion of cell cholesterol. A decrease in the red cell cholesterol corresponded to an increase in osmotic fragility. Conversely, a repletion of red cell cholesterol decreased the osmotic fragility, but the procedure did not significantly change the phospholipid contents of red cells. Accordingly, osmotic fragility of the red cells correlated highly with the cholesterol content of the cell membrane (r = -0.922, p < 0.001) and with the molar ratio of cholesterol to phospholipid in the red cells (r = -0.887, p < 0.001). Red cells incubated with plasma had decreased membrane cholesterol and increased osmotic fragility, but the change was prevented by the inactivation of lecithin cholesterol acyltransferase (LCAT) in the plasma. The above results confirm that membrane cholesterol stabilizes human and rat red cells in vitro as well as in vivo, and the content of red cell cholesterol is regulated by the exchange of plasma free cholesterol in vitro. LCAT activity in the plasma is an influential factor in controlling the cholesterol content of red cells.
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A case of transitional cell carcinoma arising from a bladder which was left behind for more than 24 years without pyocystis syndrome is described. A search in the literature revealed 10 cases of defunctionalized bladder that developed tumors over a rather short latent period ranging from 3 months to 7 years, and mostly with evidence of severe bladder infection.
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The possibility that there is some common factor in protein deprivation and splenectomy affecting the properties of red cells was examined by measuring the lipid contents of the plasma and red cells, the surgace area and spherical index of red cells, and the lecithin cholesterol acyltransferase (LCAT) activity of the plasma in intact and splenectomized rats on diets with various levels of protein. Results showed that splenectomy markedly reduced the osmotic fragility and increased the lipid content and surface area of the red cells of all dietary groups, and that decrease in the protein content of the diet gradually reduced the osmotic fragility and increased the lipid content of the red cells. A significant linear correlation was observed between osmotic fragility and the lipid content of red cells. LCAT did not influence the cholesterol level in red cell membranes because its activity in the plasma was not affected by either splenectomy or the protein content of the diet. A protein-free diet induced normaocytic anemia, but increased the lipid content and reduced the osmotic fragility of red cells. Therefore, the effect of cholesterol in increasing the surface area of red cells was not proportional in the red cells of rats on a protein-free diet. The present studies suggest that the mechanism of accumulation of cholesterol in red cells is different in protein deprivation and splenectomy. That is, in protein deprivation, increase in red cell cholesterol may result from decreased esterification of cholesterol in the plasma because of the low concentration of the substrate of LCAT, high density lipoprotein; and in splenectomized rats, the cholesterol level of the cells may not be reduced because the red cells are not exposed to the red pulp of the spleen where the pH is very low. These possibilities are supported by the finding that the osmotic fragility of the red cells decreased most and the lipid content of the cells increased most in splenectomized rats on a protein-free diet.
The causes of osmotic fragility of red cells were studied in rats. Osmotic fragility of red cells in vivo changed after removal of the spleen or induction of experimental splenomegaly by repeated intraperitoneal injections of methyl cellulose (MC): in splenectomized rats, the red cells showed reduced osmotic fragility and an increase in diameter as well as in contents of phospholipids and cholesterol. Conversely in rats with splenomegaly, the cells showed increased osmotic fragility and a decrease in diameter and in lipid contents. Results confirmed that increase in the phospholipid content resulted in decreased fragility and that increase in the cholesterol content brought about decreased spherocytosis. The activity of lecithin cholesterol acyltransferase (LCAT) in the plasma varied inversely with the cholesterol content of the red cells. The above results show that the fragility of red cells is influenced by their lipid content and shape, and that LCAT activity in the plasma influences the membrane content of cholesterol and spherocytosis.
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The sequestration of erythrocytes in rats was studied using an isologous 51Cr-labeled population of either normal or N-ethyl-maleimide (NEM) treated red cells. The spleen sequestered the damaged red cells selectively, while the liver compensated and overshot the sequestration for spleen after splenectomy. The sequestering response in liver increased gradually reaching a maximum level around 8 weeks after splenectomy and then declining toward the control level. These compensatory responses in liver were not observed in rats fed a low-protein diet, which indicated that the proliferative response imposed on liver by an extra work after splenectomy was not stimulated in the rats fed a low-protein diet. Splenectomy prolonged erythrocyte survival and reduced the osmotic fragility of normal red cells, but the compensatory increase in sequestration of damaged red cells in liver did not alter the survival and osmotic fragility of normal red cells of the rat. This fact indicates that the increased sequestration of reticuloendothelial cells in liver is basically reparative, and it is impossible to compensate for the absence of the spleen because of an inability to duplicate certain anatomic features peculiary to the spleen.
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