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.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D009202:Cardiomyopathies / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D006224:Cricetinae; D004573:Electrolytes / Q000097:blood; D004798:Enzymes / Q000097:blood; D005260:Female; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000378:metabolism
D004573:Electrolytes; D004798:Enzymes; D007545:Isoproterenol; D002118:Calcium