BACKGROUND: In congestive heart failure (CHF), function and metabolism of skeletal muscles are abnormal. AIM: To evaluate whether the reduced oxidative capacity of skeletal muscles in CHF is due to impaired O(2) utilisation. METHODS: CHF was induced in rats by injecting 50 mg/Kg monocrotaline. Several animals received the same dose of monocrotaline but only compensated right ventricular hypertrophy and no sign of congestion resulted. Two age- and diet-matched groups of control animals were also studied. In soleus and extensor digitorum longus (EDL) muscles, we studied skeletal muscle blood flow, oxidative capacity and respiratory function of skinned muscle fibres. RESULTS: In CHF, we observed a decrease of muscle blood flow (statistically significant in the soleus, p < 0.05 vs. controls). In compensated rats, a similar trend in blood flow was observed. In both soleus and EDL, a significant reduction of high energy phosphate and a shift of the redox potential towards accumulation of reducing equivalents were observed. The reduction of energy charge was not correlated to the decrease of blood flow. In skinned myofibres, the ratio of O(2) utilised in the presence and in absence of ADP (an index of phoshorilating efficiency) was reduced from 8.9 +/- 1.9 to 2.7 +/- 0.2 (p < 0.001) and from 5.7 +/- 1.0 to 2.0 +/- 0.3 (p < 0.01) in soleus and EDL, respectively. Activity of the different complexes of respiratory chain was investigated by means of specific inhibitors, showing major abnormalities at the level of complex I. In fact, inhibition of VO(2) by rotenone was decreased from 83.5 +/- 3.2 to 36.4 +/- 9.6 % (p < 0.005) and from 81.8 +/- 6.1 to 38.2 +/- 7.4 % (p < 0.005) in soleus and EDL, respectively. CONCLUSIONS: In rats with CHF, abnormalities of oxidative phosphorylation of muscles occur and complex I of the respiratory chain seem to be primarily affected. The metabolic alterations of skeletal muscles in CHF may be explained, at least in part, by an impaired O(2) utilisation.
BACKGROUND: In congestive heart failure (CHF), function and metabolism of skeletal muscles are abnormal. AIM: To evaluate whether the reduced oxidative capacity of skeletal muscles in CHF is due to impaired O(2) utilisation. METHODS:CHF was induced in rats by injecting 50 mg/Kg monocrotaline. Several animals received the same dose of monocrotaline but only compensated right ventricular hypertrophy and no sign of congestion resulted. Two age- and diet-matched groups of control animals were also studied. In soleus and extensor digitorum longus (EDL) muscles, we studied skeletal muscle blood flow, oxidative capacity and respiratory function of skinned muscle fibres. RESULTS: In CHF, we observed a decrease of muscle blood flow (statistically significant in the soleus, p < 0.05 vs. controls). In compensated rats, a similar trend in blood flow was observed. In both soleus and EDL, a significant reduction of high energy phosphate and a shift of the redox potential towards accumulation of reducing equivalents were observed. The reduction of energy charge was not correlated to the decrease of blood flow. In skinned myofibres, the ratio of O(2) utilised in the presence and in absence of ADP (an index of phoshorilating efficiency) was reduced from 8.9 +/- 1.9 to 2.7 +/- 0.2 (p < 0.001) and from 5.7 +/- 1.0 to 2.0 +/- 0.3 (p < 0.01) in soleus and EDL, respectively. Activity of the different complexes of respiratory chain was investigated by means of specific inhibitors, showing major abnormalities at the level of complex I. In fact, inhibition of VO(2) by rotenone was decreased from 83.5 +/- 3.2 to 36.4 +/- 9.6 % (p < 0.005) and from 81.8 +/- 6.1 to 38.2 +/- 7.4 % (p < 0.005) in soleus and EDL, respectively. CONCLUSIONS: In rats with CHF, abnormalities of oxidative phosphorylation of muscles occur and complex I of the respiratory chain seem to be primarily affected. The metabolic alterations of skeletal muscles in CHF may be explained, at least in part, by an impaired O(2) utilisation.
Authors: Robson Francisco Carvalho; Rafael Dariolli; Luis Antonio Justulin Junior; Mário Mateus Sugizaki; Marina Politi Okoshi; Antonio Carlos Cicogna; Sérgio Luis Felisbino; Maeli Dal Pai-Silva Journal: Int J Exp Pathol Date: 2006-12 Impact factor: 1.925
Authors: Rob C I Wüst; David S Myers; Rachel Stones; David Benoist; Philip A Robinson; John P Boyle; Chris Peers; Ed White; Harry B Rossiter Journal: Am J Physiol Heart Circ Physiol Date: 2011-10-28 Impact factor: 4.733
Authors: Xander H T Wehrens; Stephan E Lehnart; Steven Reiken; Roel van der Nagel; Raymond Morales; Jie Sun; Zhenzhuang Cheng; Shi-Xiang Deng; Leon J de Windt; Donald W Landry; Andrew R Marks Journal: Proc Natl Acad Sci U S A Date: 2005-06-22 Impact factor: 11.205
Authors: Francis da Silva Lopes; Robson Francisco Carvalho; Gerson Eduardo Rocha Campos; Mario Matheus Sugizaki; Carlos Roberto Padovani; Célia Regina Nogueira; Antonio Carlos Cicogna; Maeli Dal Pai-Silva Journal: Int J Exp Pathol Date: 2008-06 Impact factor: 1.925
Authors: Giorgio Vescovo; Chiara Castellani; Marny Fedrigo; Grazia Maria Virzì; Giovanni Maria Vescovo; Regina Tavano; Michela Pozzobon; Annalisa Angelini Journal: Data Brief Date: 2018-11-01