title: Orthotopic aortic transplantation: a rat model to study the development of chronic vasculopathy.
abstract: Research models of chronic rejection are essential to investigate pathobiological and pathophysiological processes during the development of transplant vasculopathy (TVP). The commonly used animal model for cardiovascular chronic rejection studies is the heterotopic heart transplant model performed in laboratory rodents. This model is used widely in experiments since Ono and Lindsey published their technique. To analyze the findings in the blood vessels, the heart has to be sectioned and all vessels have to be measured. Another method to investigate chronic rejection in cardiovascular questionings is the aortic transplant model. In the orthotopic aortic transplant model, the aorta can easily be histologically evaluated. The PVG-to-ACI model is especially useful for CAV studies, since acute vascular rejection is not a major confounding factor and Cyclosporin A (CsA) treatment does not prevent the development of CAV, similar to what we find in the clinical setting. A7-day period of CsA is required in this model to prevent acute rejection and to achieve long-term survival with the development of TVP. This model can also be used to investigate acute cellular rejection and media necrosis in xenogeneic models.
authors.affiliation: University Heart Center Hamburg, Transplant and Stem Cell Immunobiology Lab, University Hospital Hamburg.
authors.forename: Mandy
authors.initials: M
authors.lastname: Stubbendorff
authors.forename: Tobias
authors.initials: T
authors.lastname: Deuse
authors.forename: Anna
authors.initials: A
authors.lastname: Hammel
authors.forename: Robert C
authors.initials: RC
authors.lastname: Robbins
authors.forename: Hermann
authors.initials: H
authors.lastname: Reichenspurner
authors.forename: Sonja
authors.initials: S
authors.lastname: Schrepfer
mesh_terms: D000818:Animals; D001011:Aorta / Q000637:transplantation*; D002908:Chronic Disease; D004195:Disease Models, Animal; D006084:Graft Rejection / Q000473:pathology*; D051381:Rats; D011912:Rats, Inbred ACI; D014184:Transplantation, Homologous / Q000009:adverse effects; D014652:Vascular Diseases / Q000209:etiology* / Q000473:pathology