title: Skeletal muscle metabolism in experimental heart failure.
abstract: We studied peripheral skeletal muscle metabolism in monocrotaline-treated rats. Two distinct groups emerged: a percentage of the animals developed ventricular hypertrophy, with no signs of heart failure (compensated group), whilst others, besides ventricular hypertrophy, developed the syndrome of congestive heart failure (CFH group). Oxidative metabolism and redox cellular state were expressed in terms of creatine phosphate, purine (ATP, ADP and AMP) and pyridine (NAD and NADH) nucleotides tissue content. Skeletal muscles with different metabolism were studied: (a) Soleus (oxidative), (b) extensor digitorium longus (glycolytic) and tibialis anterior (oxidative and glycolytic). The results showed that in CFH animals a decreased high-energy phosphates content occurs in the soleus and extensor digitorum longus, but not in the tibialis anterior. In the soleus. ATP declined from 20.31 +/- 2.5 of control group to 9.55 +/- 0.61 mumol/g dry wt. while in the extensor digitorum longus ATP declined from 30.92 +/- 2.68 to 22.7 +/- 1.54 mumol/g dry wt. In both these muscles, a shift of NAD/NADH couple towards oxidation was also observed (from 26.58 +/- 3.34 to 6.95 +/- 0.97 and from 18.88 +/- 3.43 to 10.57 +/- 1.61, respectively). These alterations were more evident in the aerobic soleus muscle. On the contrary, no major changes occurred in skeletal muscle metabolism of compensated animals. The results show that: (1) a decrease in muscle high-energy phosphates occurs in CFH; (2) this is accompanied by a decrease of NAD/NADH couple suggesting an impairment in oxygen utilization or availability.
authors.affiliation: Fondazione Salvatore Maugeri, Clinica del Lavoro e della Riabilitazione, Gussago, Brescia, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Bernocchi
authors.forename: C
authors.initials: C
authors.lastname: Ceconi
authors.forename: P
authors.initials: P
authors.lastname: Pedersini
authors.forename: E
authors.initials: E
authors.lastname: Pasini
authors.forename: S
authors.initials: S
authors.lastname: Curello
authors.forename: R
authors.initials: R
authors.lastname: Ferrari
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006333:Heart Failure / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D016686:Monocrotaline / Q000494:pharmacology; D018482:Muscle, Skeletal / Q000378:metabolism*; D009243:NAD / Q000378:metabolism; D009929:Organ Size; D010084:Oxidation-Reduction; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D010725:Phosphocreatine; D009243:NAD; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D016686:Monocrotaline; D000255:Adenosine Triphosphate