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Biomedical subjects

B Solymoss

Publications and source records attributed to B Solymoss.

At least 19 recordsLinked to original sources
PubMed1979

Therapeutic trials in hamster dystrophy.

Verapamil and prenylamine, which antagonize calcium influx into heart muscle cells, Dibenamine and propanolol, alpha and beta adrenergic bockers, respectively, and prostaglandin E1, which acts on permeability of cell membranes and on adrenergic neurotransmission, were all shown to markedly reduce the severity of heart lesions in UM-X7.1 cardiomyopathic hamsters. The beneficial effects of these compounds seen essentially preventive, in that they do not afford protection for fully developed skeletal muscle lesions. The occurrence of the pathologic changes in the myocardium coincides with an increased adrenergic nerve activity, and it is believed that these drugs function mainly by decreasing calcium conductivity across the sarcolemmal membranes of cardiocytes.

Animals↗
PubMed1979

Metaplastic and mitotic activity of the ischemic (endocrine) kidney in experimental renal hypertension.

Partial ligation of the aorta between the renal arteries in the rat induces malignant hypertension, metaplasia of smooth-muscle cells of arterioles and arteries into juxtaglomerular cells, and a complex series of events in tubular cells at all levels of the ischemic kidney. The tubular cells of the outer cortex, particularly the proximal convoluted cells, show a very rapid and progressive simple atrophy. In contrast, necrosis of individual cells is followed by mitotic activity in atrophic tubular cells of the inner cortex, medulla, and papilla. Subsequently, polyploidy and hyperplasia occur in the inner cortex. At the same time, hypertrophy of the protein-synthesizing apparatus and an increase in protein, DNA, and RNA, followed by a decrease in the protein content, are seen in the tubular cells of the inner cortex. In the medulla and papilla, necrosis of individual cells proceeds side by side with waves of mitotic activity. These events take place, albeit to a lesser degree, even in cases of very mild renal ischemia. While they may by unrelated to hypertension, these changes are probably involved in the increase in hydrolytic enzyme activity characteristic of the ischemic renal cortex.

Animals↗
PubMed1978

Studies of the mechanism of polycythemia induced in rats by Ni3S2.

Intrarenal injection of 10 mg Ni3S2 elicits polycythemia in rats. This can be attributed either to direct stimulation or to erythropoietin-induced hyperplasia of erythropoietic elements of bone marrow. While studying the mechanism of this experimental model of polycythemia we noted that: (a) extirpation of the injected kidney after the development of the hematologic alterations abolished the polycythemia within 1 month; (b) intravenous, intramuscular or intrahepatic treatment with Ni3S2 was ineffective in producing polycythemia; and (c) there was a modest but statistically significant elevation of plasma erythropoietin levels in rats 2,4 and 8 weeks after injection of Ni3S2, at a time when the hematocrit values were increased. The experiments support the view that Ni3S2 does not directly stimulate erythropoiesis in bone marrow but primarily affects the injected kidney, which in turn (by the continuous liberation of modest amounts of erythropoietin or some hitherto unknown substance) triggers the development of polycythemia.

Animals↗
PubMed1975

On the mechanism of polychlorinated biphenyl-induced hypobilirubinaemia.

Treatment of normal rats with a polychlorinated biphenyl mixture of DDT increased liver microsomal protein concentration. Hepatic microsomal bilirubin UDP-glucuronyltransferase activity was elevated in the DDT-treated, but not in the polychlorinated biphenyl-treated rats. In contrast polychlorinated biphenyl, but not DDT, reduced serum bilirubin concentrations in jaundiced Gunn rats, as did sulphadiazine; sulphonamides compete with bilirubin for binding sites on plasma albumin. Polychlorinated biphenyls appear to lower serum bilirubin concentration by reducing the binding of bilirubin to plasma protein.

Animals↗
PubMed1975

Polycythemia induced in rats by intrarenal injection of nickel sulfide Ni3S2.

In rats, injection of nickel sulfide (5 mg) into each pole of one kidney, unlike intramuscular administration, elicits a plethoric condition a few weeks later. The resulting hematologic changes (increased hematocrit, hemoglobin, erythrocytes and circulating erythrocyte mass with normal plasma volume) indicate that the plethoric condition is due to polycythemia, which is not associated with alterations in the 2,3-diphosphoglyceric acid content of erythrocytes. Removal of the treated kidney, following the development of the polycythemia, as well as the tumor growth and expansion in the renal parenchyma, reverse the plethoric condition, suggesting that the erythropoietic changes derive from nickel-induced renal lesions. Further studies are required to elucidate the nature and mechanisms of the cellular alterations.

Animals↗
PubMed1975

Prevention of hereditary cardiomyopathy in the hamster by verapamil and other agents.

Verapamil, Prenylamine and, to a lesser extent, Cinnarizine were highly efficient in preventing the development or reducing the severity of heart lesions in cardiomyopathic hamster of the UM-X7.1 line. The calcium antagonistic compounds did not protect against the skeletal muscle changes already present at the time when treatment was initiated. The cardiac lesions were also significantly diminished in frequency and severity by a low calcium diet and in apparent contradiction, by parenteral administration of calcium gluconate. The relation of these electrolytes and creatine phosphokinase is not yet fully understood but suggests that a primary defect in muscles cell membranes may be responsible for hereditary cardiomyopathy in hamsters.

Animals↗
PubMed1975

Effect of fasting, phenobarbital, or hydrocortisone on serum creatine-phosphokinase and aldolase activity in myopathic Syrian hamsters.

The hereditary polymyopathy and cardiomyopathy of inbred Syrian hamsters (UM X 7.1) are associated with a marked elevation of serum creatine phosphokinase (CPK) and aldolase levels. Fasting (overnight) further increases (+100-500%) the serum concentration of these enzymes in myopathic hamsters; however, no such effect is demonstrable in normal hamsters, or in first generation offspring produced by crossbreeding the two strains (myopathic and normal). The changes are reversible, and the enzyme values return to previous levels within 72 hr. Neither phenobarbital nor hydrocortisone prevents the rises, as shown by CPK determinations; on the contrary, hydrocortisone elicits even greater serum enzyme increases.

Animals↗
PubMed1975

Effect of thyroparathyroidectomy and of a low calcium diet on the cardiomyopathy of the Syrian hamster.

Experimental Ca deficiency in the cardiomyopathic Syrian hamster was found to be effective in reducing the incidence and the severity of the heart lesions that develop at 30 days of age. The skeletal muscle changes that develop at a much earlier period were influenced in their course but not in their frequency. It was further observed that 20-day-old animals benefit better from a low Ca intake at a time when the degenerative changes do not prevail in the myocardium. Removal of the parathyroids in normally fed myopathic hamsters had no effect on the serum calcium and phosphate levels or on the course of the disease. The serum creatine phosphokinase was found to be higher in Ca-deficient myopathic hamsters. The possible role of calcium concerning the maintenance of the integrity of the muscle cells is discussed.

Animals↗