title: Cell transplantation to prevent heart failure: a comparison of cell types.
abstract: BACKGROUND
  Autologous cell transplantation may restore viable muscle after a myocardial infarction. We compared the effect of three cell types or an angiotensin-converting enzyme (ACE) inhibitor on preservation of ventricular function after cardiac injury.
  
  
  METHODS
  A uniform transmural myocardial scar was created in adult rats by cryoinjury. Three weeks later the rats were randomly assigned to one of four blinded treatments: transplantation with 5 x 10(6) aortic smooth muscle cells (SMC, n = 12), ventricular heart cells (VHC, n = 13), skeletal muscle cells (SKC, n = 13) or culture medium alone (control, n = 11). The ACE inhibitor group (n = 8) received enalapril (1.0 mg/kg per day), also beginning 3 weeks after cryoinjury. Five and 12 weeks after transplantation, left ventricle (LV) function was assessed in a Langendorff apparatus, and histologic and immunohistological evaluation of the LV scars was performed.
  
  
  RESULTS
  At 5 weeks, greater scar elastin content and better LV function was noted with cell transplantation or ACE inhibitor therapy compared with control rats (p < 0.05). Twelve weeks after transplantation, cell-transplanted rats still had greater elastin content and better LV function than control rats, although elastin content and LV function had declined in ACE inhibitor-treated animals to levels below those observed in control rats (p < 0.05).
  
  
  CONCLUSIONS
  Transplantation of SMC, VHC, and SKC preserved ventricular function equivalent to the effects of an ACE inhibitor. Muscle cell transplantation, but not ACE inhibitor therapy, continues to be effective later after cryoinjury. No differences were detected between the muscle cells.
authors.affiliation: Department of Surgery, Division of Cardiovascular Surgery, Toronto General Research Institute, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada.
authors.forename: Takeshiro
authors.initials: T
authors.lastname: Fujii
authors.forename: Terrence M
authors.initials: TM
authors.lastname: Yau
authors.forename: Richard D
authors.initials: RD
authors.lastname: Weisel
authors.forename: Nobuhisa
authors.initials: N
authors.lastname: Ohno
authors.forename: Donald A G
authors.initials: DA
authors.lastname: Mickle
authors.forename: Noritsugu
authors.initials: N
authors.lastname: Shiono
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Ozawa
authors.forename: Keiji
authors.initials: K
authors.lastname: Matsubayashi
authors.forename: Ren-Ke
authors.initials: RK
authors.lastname: Li
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000166:cytology; D002303:Cardiac Output, Low / Q000209:etiology / Q000517:prevention & control; D017690:Cell Transplantation; D002478:Cells, Cultured; D002921:Cicatrix / Q000378:metabolism; D015925:Cryopreservation; D004549:Elastin / Q000032:analysis; D004656:Enalapril / Q000494:pharmacology; D006335:Heart Injuries / Q000150:complications / Q000628:therapy; D006352:Heart Ventricles / Q000166:cytology / Q000378:metabolism; D007150:Immunohistochemistry; D018482:Muscle, Skeletal / Q000166:cytology; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D009203:Myocardial Infarction / Q000150:complications / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000737:chemistry; D051381:Rats; D011917:Rats, Inbred Lew; D016277:Ventricular Function, Left
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D004656:Enalapril; D004549:Elastin