title: Differential myolysis of myocardium and skeletal muscle in hamsters with dilated cardiomyopathy: beneficial protective effect of diltiazem.
abstract: BACKGROUND
  Although dilated cardiomyopathic hamsters (TO-2) with mutation of the delta-sarcoglycan gene exhibit histological features of muscular dystrophy, it remains to be elucidated whether both myocardium and skeletal muscle are injured in a similar manner.
  
  
  RESULTS
  The progression of myolysis in both myocardium and skeletal muscle were assessed biochemically and pathologically in TO-2 and F1B control hamsters. Left ventricular (LV) function was assessed by echocardiography and cardiac catheterization. Both the plasma concentration of cardiac troponin T and the plasma activity of alpha-hydroxybutyrate dehydrogenase (HBD) peaked at 8 weeks of age, and thereafter reduced greatly in TO-2 hamsters. Activity of creatine kinase (CK) in TO-2 hamsters was significantly greater than in controls throughout the observation period. Pathological findings of both nuclear chain and central nuclei in skeletal muscles were observed in TO-2 hamsters throughout the observation period, suggesting regeneration. LV dysfunction was first evident at 8 weeks of age and deteriorated thereafter in TO-2 hamsters. Treatment of TO-2 hamsters with diltiazem from 5 to 8 weeks of age could avert the LV functional deterioration and the increment in alpha-HBD activity, but CK activity was unchanged.
  
  
  CONCLUSIONS
  Despite myolysis in skeletal muscle occurring consistently throughout the observation period, cardiac myolysis occurred predominantly in the early phase. These initial cardiac events might involve coronary spasm and/or calcium overload in the myocardium.
authors.affiliation: Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Kato
authors.forename: Mitsunori
authors.initials: M
authors.lastname: Iwase
authors.forename: Kenji
authors.initials: K
authors.lastname: Takagi
authors.forename: Takao
authors.initials: T
authors.lastname: Nishizawa
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kanazawa
authors.forename: Aya
authors.initials: A
authors.lastname: Matsushita
authors.forename: Hisashi
authors.initials: H
authors.lastname: Umeda
authors.forename: Hideo
authors.initials: H
authors.lastname: Izawa
authors.forename: Akiko
authors.initials: A
authors.lastname: Noda
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Koike
authors.forename: Kohzo
authors.initials: K
authors.lastname: Nagata
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yokota
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D002311:Cardiomyopathy, Dilated / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D003402:Creatine Kinase / Q000097:blood; D006224:Cricetinae; D004110:Diltiazem / Q000494:pharmacology / Q000627:therapeutic use*; D004453:Echoencephalography; D005786:Gene Expression Regulation / Q000235:genetics / Q000502:physiology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006884:Hydroxybutyrate Dehydrogenase / Q000097:blood; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D009154:Mutation; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D049031:Sarcoglycans / Q000235:genetics / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000473:pathology / Q000503:physiopathology
chemical_list: D002121:Calcium Channel Blockers; D049031:Sarcoglycans; D006884:Hydroxybutyrate Dehydrogenase; D003402:Creatine Kinase; D004110:Diltiazem