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Biomedical subjects

G Jasmin

Publications and source records attributed to G Jasmin.

At least 73 records · Page 4Linked to original sources
PubMed1979

Cardiomyopathy of hamster dystrophy.

Investigations of the fine structural changes observed in the hearts of cardiomyopathic hamsters at very early stages of the disease indicate that the initial changes involve the pericapillary mesenchymal cells. Other prominent features consist of hypercontraction of cardiocytes, disruption of intercalated disks, and eventual partitioning of cardiac cells, with myofibrillar lysis. The generalized plasma membrane defect allows a net increase in calcium influx and a depression in mitochondrial respiratory control ratios. These pathologic events are in accord with previously reported increases in myocardial sympathic nerve activity.

Animals↗
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

[Type 1 fucosidosis. Anatomical study].

The first Canadian child with complete absence of alpha L-fucosidase is described. The neurological course was characterised by rapid deterioration and he died at the earliest age recorded so far. There are only two published reports of autopsies in this condition to which we add another, together with the ultrastructural findings of a liver biopsy.

Autopsy↗
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↗
PubMed1976

Comparison of heart sarcolemmal enzyme activities in normal and cardiomyopathic (UM-X7.1) hamsters.

1. The activities of some membrane-bound enzymes such as adenylate cyclase, Na+ + K+-stimulated adenosine triphosphatase (Na+ + K+-ATPase), Ca2+-stimulated ATPase and Mg2+-stimulated ATPase were examined in heart sarcolemmal fractions from control and cardiomyopathic hamsters at different stages of heart failure. 2. The basal adenylate cyclase activity in sarcolemma from cardiomyopathic animals with early, moderate and late stages of heart failure was not different from the control values whereas the sodium fluoride- and catecholamine-stimulated adenylate cyclase activities were depressed in cardiomyopathic sarcolemma at moderate and late stages. 3. The sarcolemmal Na+ + K+-ATPase activity was decreased and the non-specific phosphatase activity was increased at early, moderate and late stages of heart failure. 4. The sarcolemmal Ca2+-ATPase activity was decreased at moderate and late stages whereas the Mg2+-ATPase activity was decreased at the late stages of heart failure only. 5. A marked decrease was found in calcium binding by heart sarcolemma from cardiomyopathic hamsters at late stages of failure. 6. These results suggest that dramatic sarcolemmal changes are associated with heart failure, and support the view that membrane abnormalities play a crucial role in the development of myocardial dysfunction, cyclase, calcium binding, heart failure, heart membranes, sarcolemmal enzymes.

Adenosine Triphosphatases↗
PubMed1976

Renal carcinomas and erythrocytosis in rats following intrarenal injection of nickel subsulfide.

In rats, an intrarenal injection of nickel subsulfide (Ni3S2) regularly caused, within 2 months, an erythrocytosis and eventually a renal carcinoma in 40 per cent of the animals. Despite their great pleomorphism, the neoplastic renal cells appeared to be of the same lineage but showed a pronounced tendency to evolve toward an anaplastic, spindle-cell variant. By electron microscopy, they exhibited varying degrees of differentiation with surface specialization, suggesting an epithelial origin. There was no indication that the erythrogenic and carcinogenic responses to Ni3S2 were interrelated as the high hemoglobin and erythrocyte values tended to retrocede with the development of the renal carcinoma. Other nickel salts and a variety of divalent metallic preparations failed to produce similar changes when administered under identical conditions. The possible mechanism of NI3S2 at the cellular level is briefly discussed.

Animals↗
PubMed1975

Defective membrane systems in dystrophic skeletal muscle of the UM-X7.1 strain of genetically myopathic hamster.

1. The function of mitochondria, sarcotubular membranes (heavy microsomes), sarcolemma and myofibrils from the hind-leg skeletal muscle of about 60- and 150-day-old normal and myopathic (UM-X7.1) hamsters was examined. 2. The mitochondrial calcium uptake as well as mitochondrial phosphorylation and respiratory rates were lower in 60-day-old myopathic skeletal muscle, unlike 150-day-old myopathic animals, when pyruvate-malate and glutamate-malate were used as substrates. However, mitochondria from 150-day-old myopathic animals showed depressed glutamate-dependent respiratory and phosphorylation rates and succinate-supported initial rate of calcium uptake. 3. The microsomal calcium-uptake, but not calcium-binding, and Ca2+-stimulated adenosine triphosphatase (ATPase) activity of the 150-day-old myopathic skeletal muscle were lower than the control values. Although microsomal calcium-binding, calcium-uptake and ATPase activities of the 60-day-old myopathic muscle were not depressed significantly, the initial rate of calcium uptake was less than the control. 4. The sarcolemmal Ca2+-ATPase, but not Mg2+-ATPase or Na+ +K+-ATPase, activity was higher in 60-day-old myopathic muscle whereas the activities of all these enzymes from 150-day-old myopathic animals were higher than the control. On the other hand, the Na+ +K+-ATPase activities from 60- and 150-day-old myopathic animals were inhibited by ouabain to a lesser extent in comparison with the respective control values. 5. The myofibrillar Ca2+-ATPase and Mg2+-ATPase activities as well as inhibition of Mg2+-ATPase due to Na+ and K+ in myopathic muscle were no different from the control values. 6. The results reported here give further support to the view that different membrane systems of the dystrophic muscle are defective.

Adenosine Triphosphatases↗
PubMed1975

Studies on adenylate cyclase-cyclic AMP system of the myopathic hamster (UM-X7.1) skeletal and cardiac muscles.

Cyclic AMP content, adenylate cyclase (EC 4.6.1.1) activity and phosphodiesterase I (EC 3.1.4.1) activity of the hind leg skeletal muscle and cardiac muscle in 60- and 150-day-old normal and myopathic (UM-X7.1) hamsters were examined. In 60-day-old myopathic animals, cardiac cyclic AMP levels were higher and phosphodiesterase I activity was lower, without any changes in the basal adenylate cyclase activity, whereas in 150-day-old myopathic hamsters, cardiac cyclic AMP and basal adenylate cyclase activity were lower, without any changes in the homogenate phosphodiesterase I activity. On the other hand, basal adenylate cyclase and phosphodiesterase I activities in the skeletal muscle homogenate from 60- and 150-day-old myopathic animals were not different from the normal values but the skeletal muscle cyclic AMP levels were significantly less in 60-day-old myopathic hamsters only. The plasma cyclic AMP levels in 60-day-old myopathic hamsters, unlike 150-day-old myopathic animals, were higher than the normal. Although these results reveal differences in myopathic cardiac and skeletal muscles, it is concluded that changes in adenylate cyclase-cyclic AMP system in myopathy are dependent upon the degree of disease.

Adenylyl Cyclases↗
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

Prevention of myocardial generation in hamsters with hereditary cardiomyopathy.

A number of drugs have been tested for their ability to prevent or change the course of skeletal and heart lesions occurring with a 100% incidence in cardiomyopathic hamsters (UM-X7.1). These drugs were selected because they act either on the metabolism or turnover of Ca or on adrenergic receptors. Verapamil (Isoptin), a potent inhibitor of myocardial transmembrane Ca conductivity, was found to completely prevent the myocardial lesions in myopathic hamsters. The hamsters were 28 to 30 days of age at the beginning of the experiment and were injected subcutaneously twice daily during 30 consecutive days in doses of 0.5 mg during the first week and 0.75 mg during the subsequent weeks. The protection afforded by Verapamil was no longer evident 30 days after interruption of the treatment. The severity of both cardiac and skeletal muscle lesions was found significantly lowered in hamsters receiving Dibenamine. It is assumed that Verapamil acts mainly by preventing excessive calcium influx in cardiomyocytes, whereas Dibenamine improves the microcirculation, which is deficient during the necrotizing phase of the polymyopathy. The latter assumption rests on the fact that, in myopathic hamsters, the reactivity pattern of alkaline phosphatase is altered at the level of the capillaries of cardiac and skeletal muscles.

Alkaline Phosphatase↗
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↗
PubMed1975

Membrane alteration in failing hearts of cardiomyopathic hamsters.

Cardiomyopathic hamsters (UM-X7.1) show clinical signs of congestive heart failure and an abnormal EKG pattern. The sarcolemmal fraction obtained from the failing hearts at advanced stages of myopathy exhibited no change in the basal adenylate cyclase activity; however, the activity of this enzyme in the presence of catecholamines or NaF was lower in the failing heart sarcolemma than that in the control. The activities of Ca2+-ATPase, Mg2+-ATPase, and Na+-K+-ATPase in the failing heart sarcolemma were also less than the control values. These results suggest an association of membrane defect with heart failure.

Adenosine Triphosphatases↗
PubMed1975

[Changes in the muscle fiber induced by p-phenylenediamine in the rat].

P-phenylenediamine (PPD) induces skeletal muscle lesions in rats which have been chosen as a model for investigation of the inflammatory and degenerative pattern of the muscle fibers. With the use of histochemical and ultrastructural criteria, the morphology of the lesions have been analysed in the diaphragm. Fifteen minutes after the induction by PPD, a subsarclemmal oedema can be shown by electron microscopy. Enzymatic changes appear during the first hour. The pathologic features are more prominent after twenty-four hours. The lesions are characterized by a segmental necrosis adjacent to unaltered fibers and by particular types of fibers such as target, snake coils, core fiber. A comparison between the lesions induced by PPD and those occurring during other types of myopathies has been made.

Adenosine Triphosphatases↗