title: Oxidative stress and nitric oxide synthase in skeletal muscles of rats with post-infarction, compensated chronic heart failure.
abstract: OBJECTIVE
  Involvement of oxidative stress and nitric oxide synthase (NOS) isoforms in skeletal muscle cellular adaptations to chronic heart failure (CHF) is controversial, and possible muscle fibre-type heterogeneity in the oxidative stress and NOS responses to CHF have not been examined. Consequently, we hypothesized that the changes in determinants of elevated oxidative and nitrosylative stress associated with CHF would occur in skeletal muscle and would be similar in predominantly type I slow twitch muscle (soleus) and type II fast twitch muscle (plantaris) of rats.
  
  
  METHODS
  The purpose of this study was to measure NOS isoforms (endothelial, inducible and neuronal NOS) and antioxidant enzymes (SOD-1, SOD-2, catalase) by protein immunoblot as well as markers of oxidative stress by biochemical assays in soleus and plantaris muscle sections of the rat hind limb. This was performed for control and post-infarction, compensated CHF rats.
  
  
  RESULTS
  Twelve weeks after coronary artery ligation-induced moderate CHF, soleus exhibited decreased SOD-1, SOD-2 and eNOS, but increased iNOS and nNOS isoforms assessed by immunoblot. This was associated with elevated lipid and DNA oxidative damage assessed by biochemical assays. In contrast, plantaris muscle exhibited no changes in antioxidant enzymes or NOS isoforms, and had lower lipid and DNA oxidative damage.
  
  
  CONCLUSIONS
  These observations suggest a heretofore unreported muscle fibre-type-specific response of oxidative stress and NOS isoforms to CHF is of importance in understanding the cellular mechanisms of skeletal muscle dysfunction in CHF.
authors.affiliation: Department of Kinesiology, University of Waterloo, Waterloo, ON, Canada. jwerush@uwaterloo.ca
authors.forename: J W E
authors.initials: JW
authors.lastname: Rush
authors.forename: H J
authors.initials: HJ
authors.lastname: Green
authors.forename: D A
authors.initials: DA
authors.lastname: Maclean
authors.forename: L M
authors.initials: LM
authors.lastname: Code
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D004249:DNA Damage; D005978:Glutathione / Q000097:blood; D006333:Heart Failure / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D015151:Immunoblotting; D015227:Lipid Peroxidation; D008297:Male; D018656:Muscle Fibers, Fast-Twitch / Q000201:enzymology / Q000473:pathology; D018485:Muscle Fibers, Skeletal / Q000201:enzymology* / Q000473:pathology; D018657:Muscle Fibers, Slow-Twitch / Q000201:enzymology / Q000473:pathology; D018482:Muscle, Skeletal / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D009203:Myocardial Infarction / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D019001:Nitric Oxide Synthase / Q000032:analysis*; D018384:Oxidative Stress; D007703:Peptidyl-Dipeptidase A / Q000032:analysis / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D019001:Nitric Oxide Synthase; D007703:Peptidyl-Dipeptidase A; D005978:Glutathione