title: Histopathologic time course of myocardial infarct in rabbit hearts.
abstract: BACKGROUND
  The histopathologic evolution of myocardial infarct and of remote zones in rabbit hearts was studied.
  
  
  METHODS
  The left coronary artery of 55 rabbits was ligated and rabbits were sacrificed at 2, 4, 6, 8, 12, 14, 16, 18, 26, 35 and 56 days post-ligature (n=5 per group). Two rabbits were used as control and four were sham-operated. The hearts were excised, cut in slices and stained with hematoxylin-eosin, Masson's trichrome and picrosirius red. The histological evaluation was semiquantitative (scale: 0 to ++).
  
  
  RESULTS
  At day 2, the presence of neutrophils was ++, decreasing suddenly at day 4 and disappearing completely at day 6. The proliferation of cells with features of fibroblasts increased from days 4 to 14 post-occlusion. Coagulation necrosis in mid-myocardium during the first week was ++. Subendocardial myocytolysis was evident from day 2 up to day 56 post-infarction. During the second week, proliferation of lymphocytes and macrophages (++), granulation tissue formation (++) and incipient traces of fibrosis that peaked at day 35 were observed. Scarring was complete at day 56 (++). In remote zones (right ventricle and septum), the proliferation of cells+ on Vimentin was observed at day 2, and perivascular, interstitial and endocardial fibrosis started to increase at day 6 and peaked at day 16.
  
  
  CONCLUSIONS
  Although myocardial infarction in rabbits maintains the essence of the infarct chronology, some differences as the early presence of cells+ on Vimentin and subendocardial fibrosis in infarcted areas, and also the rapid increase and early disappearance of neutrophils appear when other species are considered. An interesting finding was the early proliferation of cells with features of fibroblasts in remote zones.
authors.affiliation: Departamento de Patología, Facultad de Medicina, Universidad de Buenos Aires, Uriburu 950, 1114, Buenos Aires, Argentina. mmorales@fmed.uba.ar
authors.forename: Celina
authors.initials: C
authors.lastname: Morales
authors.forename: Germán E
authors.initials: GE
authors.lastname: González
authors.forename: Manuel
authors.initials: M
authors.lastname: Rodríguez
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Bertolasi
authors.forename: Ricardo J
authors.initials: RJ
authors.lastname: Gelpi
mesh_terms: D000818:Animals; D002921:Cicatrix / Q000473:pathology; D004195:Disease Models, Animal; D004699:Endocardium / Q000473:pathology; D005347:Fibroblasts / Q000473:pathology; D005355:Fibrosis / Q000473:pathology; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D009504:Neutrophils / Q000473:pathology; D011817:Rabbits; D016037:Single-Blind Method; D013997:Time Factors; D014746:Vimentin / Q000378:metabolism
chemical_list: D014746:Vimentin