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.
D000818:Animals; D001835:Body Weight; D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009202:Cardiomyopathies / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D002462:Cell Membrane / Q000378:metabolism; D002936:Cinnarizine / Q000494:pharmacology / Q000627:therapeutic use; D003402:Creatine Kinase / Q000097:blood; D006224:Cricetinae; D004573:Electrolytes / Q000097:blood; D005260:Female; D005942:Gluconates / Q000494:pharmacology; D008297:Male; D009132:Muscles / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D011299:Prenylamine / Q000494:pharmacology / Q000627:therapeutic use; D014700:Verapamil / Q000627:therapeutic use*
D004573:Electrolytes; D005942:Gluconates; D002936:Cinnarizine; D014700:Verapamil; D003402:Creatine Kinase; D011299:Prenylamine; D002118:Calcium