Quantitative procedures for cell dissociation, selective plating, and growth conditions were adapted to neonatal hamster muscle in order to obtain cultures with a predictable evolution and sufficient differentiated myofibers. Normal and myopathic cultures were compared with regard to cell yield, myogenic cell fusion, and muscle differentiation. This technique is proposed for comparative studies of in vitro myogenesis in normal and myopathic hamsters.

Animals↗

PubMedDate not supplied

Paradoxical effect of isoproterenol on hamster hereditary polymyopathy.

Isoproterenol (ISO), a potent beta-adrenoreceptor agonist, was found to interfere with the development and progression of hamster hereditary polymyopathy. Cytoprotection involved both skeletal and heart muscles with reduced myofibrillar degeneration, phagocytosis, and an unusual scarring process rarely seen at this stage of the disease. A decrease in the Ca content of heart and hemidiaphragm homogenates corroborated these findings. The significant drop of serum creatine kinase with restoration of alkaline phosphatase activity towards normal values provided additional support to the therapeutic effect of ISO. Except for an increase in magnesium, there were no changes in serum electrolytes. The modifications in plasma membrane permeability together with improvement in microcirculation are some of the features whereby ISO can ameliorate muscle cell energy metabolism. It is inferred that the alleged primary role of calcium in the development of this inherited myopathy should be further scrutinized.

Animals↗

PubMedDate not supplied

Impairment of mitochondrial and sarcoplasmic reticular functions during the development of heart failure in cardiomyopathic (UM-X7.1) hamsters.

The oxidative phosphorylation as well as calcium transporting properties of heart mitochondria and calcium transport activities of the fragments of the sarcoplasmic reticulum (microsomes) were studied during the life span of cardiomyopathic hamsters (UM-X7.1). Control healthy hamsters of the same age group were used for comparison. No changes in the oxidative phosphorylation ability of cardiomyopathic mitochondria were seen at early and moderate stages of heart failure; however, at severe stages, mitochondrial respiratory functions, but not the ADP:0 ratio, were impaired. Both creatine phosphate and ATP contents were decreased without any significant changes in the ATPase activities of myofibrils from the failing hearts. Heart mitochondria from cardiomyopathic animals at severe stages of failure exhibited less calcium binding and uptake activities in comparison with the control values whereas no changes in the mitochondrial calcium binding and uptake were seen in cardiomyopathic hamsters which showed no clinical signs of heart failure. Although mitochondrial calcium binding in cardiomyopathic hearts at early and moderate stages of failure was decreased, mitochondrial calcium uptake was not significantly different from the control. Microsomal calcium binding activity, unlike calcium uptake activity, was decreased in the hearts of cardiomyopathic hamsters without any signs of heart failure. Both calcium binding and calcium uptake activities of microsomes from animals with early, moderate and severe heart failure were less in comparison with the control values but were not associated with any changes in the Ca2+-stimulated ATPase activity. These results suggest that changes in the process of mitochondrial energy production and mitochondrial Ca2+-transport may be secondary to other factors whereas alterations in the sarcoplasmic reticular Ca2+-transport may lead to the development of heart failure in the cardiomyopathic hamsters.

Adenosine Triphosphatases↗

PubMedDate not supplied

[Polymyopathy and hereditary cardiomyopathy in the Syrian hamster. Selective inhibition of myocardial lesions].

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Adrenergic beta-Antagonists↗