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.
D000818:Animals; D006224:Cricetinae; D003983:Dibenzylchlorethamine / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D009137:Muscular Dystrophy, Animal / Q000188:drug therapy* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D011299:Prenylamine / Q000494:pharmacology / Q000627:therapeutic use*; D011433:Propranolol / Q000494:pharmacology / Q000627:therapeutic use*; D011458:Prostaglandins E / Q000494:pharmacology / Q000627:therapeutic use*; D014700:Verapamil / Q000494:pharmacology / Q000627:therapeutic use*
D011458:Prostaglandins E; D003983:Dibenzylchlorethamine; D011433:Propranolol; D014700:Verapamil; D011299:Prenylamine