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A comparative study of myocardial function and morphology during fasting/refeeding and food restriction in rats

Abstract Background This study compared the influence of fasting/refeeding cycles and food restriction on rat myocardial performance and morphology. Methods Sixty-day-old male Wistar rats were submitted to food ad libitum (C), 50% food restriction (R50), and fasting/refeeding cycles (RF) for 12 week...

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Published in:Cardiovascular pathology 2010-09, Vol.19 (5), p.e175-e182
Main Authors: Pinotti, Matheus Fécchio, Leopoldo, André Soares, Silva, Maeli Dal-Pai, Sugizaki, Mário Mateus, do Nascimento, André Ferreira, Lima-Leopoldo, Ana Paula, Aragon, Flávio Ferrari, Padovani, Carlos Roberto, Cicogna, Antonio Carlos
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Language:English
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Summary:Abstract Background This study compared the influence of fasting/refeeding cycles and food restriction on rat myocardial performance and morphology. Methods Sixty-day-old male Wistar rats were submitted to food ad libitum (C), 50% food restriction (R50), and fasting/refeeding cycles (RF) for 12 weeks. Myocardial function was evaluated under baseline conditions and after progressive increase in calcium and isoproterenol. Myocardium ultrastructure was examined in the papillary muscle. Results Fasting/refeeding cycles maintained rat body weight and left ventricle weight between control and food-restricted rats. Under baseline conditions, the time to peak tension (TPT) was more prolonged in R50 than in RF and C rats. Furthermore, the maximum tension decline rate (−d T /d t ) increased less in R50 than in RF with calcium elevation. While the R50 group showed focal changes in many muscle fibers, such as the disorganization or loss of myofilaments, polymorphic mitochondria with disrupted cristae, and irregular appearance or infolding of the plasma membrane, the RF rats displayed few alterations such as loss or disorganization of myofibrils. Conclusion Food restriction promotes myocardial dysfunction, not observed in RF rats, and higher morphological damage than with fasting/refeeding. The increase in TPT may be attributed possibly to the disorganization and loss of myofibrils; however, the mechanisms responsible for the alteration in −d T /d t in R50 needs to be further clarified.
ISSN:1054-8807
1879-1336
DOI:10.1016/j.carpath.2009.08.001