title: Trypanosoma cruzi infection induces morphological reorganization of the myocardium parenchyma and stroma, and modifies the mechanical properties of atrial and ventricular cardiomyocytes in rats.
abstract: BACKGROUND
  This study investigates morphofunctional adaptations of the heart stroma and parenchyma in rats that are chronically infected with Trypanosoma cruzi.
  
  
  METHODS
  Four-month-old male Wistar rats were randomized into control (n=14) and infected (n=14) groups. Infected animals were inoculated with T. cruzi Y strain. After 9 weeks, the animals were euthanized, and the right atrium (RA) and left ventricle (LV) were removed for biochemical, stereological, and cardiomyocyte mechanical analyses.
  
  
  RESULTS
  Infected animals presented cardiomyocyte atrophy and myocardial fibrosis. For these animals, the total volume, length, surface area, and cross-sectional area of cardiomyocytes were significantly reduced, and the total interstitial and collagen volumes were significantly increased in the RA and LV compared to the controls. The total volume and length of blood vessels were significantly increased in the LV, and the total blood vessel surface area was significantly higher in the RA of infected animals. RA and LV cardiomyocytes from infected animals exhibited a significant reduction in cell shortening (43.02% and 24.98%, respectively), prolongation of the time to the peak of contraction (17.09%) and the time to half relaxation (23.68%) compared to non-infected animals. Lipid hydroperoxides, but not mineral concentrations, were significantly increased in the RA and LV from infected animals, showing an inverse correlation with cell shortening.
  
  
  CONCLUSIONS
  T. cruzi infection induces global structural remodeling of the RA and LV in rats. This remodeling coexists with cardiomyocyte contractility dysfunction, which is possibly related to the abnormal organization of the myocardial stroma and increased cellular lipid peroxidation.
authors.affiliation: Department of General Biology, Federal University of Viçosa, MG, 36570-000, Brazil.
authors.forename: Rômulo D
authors.initials: RD
authors.lastname: Novaes
authors.forename: Arlete R
authors.initials: AR
authors.lastname: Penitente
authors.forename: Reggiani V
authors.initials: RV
authors.lastname: Gonçalves
authors.forename: André
authors.initials: A
authors.lastname: Talvani
authors.forename: Maria C G
authors.initials: MC
authors.lastname: Peluzio
authors.forename: Clóvis A
authors.initials: CA
authors.lastname: Neves
authors.forename: Antônio J
authors.initials: AJ
authors.lastname: Natali
authors.forename: Izabel R S C
authors.initials: IR
authors.lastname: Maldonado
mesh_terms: D000818:Animals; D001284:Atrophy; D048430:Cell Shape; D002598:Chagas Cardiomyopathy / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology / Q000821:virology; D003331:Coronary Vessels / Q000473:pathology / Q000821:virology; D004195:Disease Models, Animal; D005355:Fibrosis; D006325:Heart Atria / Q000473:pathology / Q000821:virology; D006352:Heart Ventricles / Q000473:pathology / Q000821:virology; D015227:Lipid Peroxidation; D008297:Male; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D051381:Rats; D017208:Rats, Wistar; D017154:Stromal Cells / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D013997:Time Factors; D014349:Trypanosoma cruzi / Q000472:pathogenicity*; D020257:Ventricular Remodeling; D014774:Virulence
keywords: Cardiac myocytes; Chagas' disease; Extracellular matrix; Oxidative stress; Pathology; X-ray spectroscopy