TY - JOUR
T1 - Fisher-Lewis Kidney Transplantation Model as a Tool for Investigation of Transplantation-Induced Cardiomyopathy
AU - Baumann, M.
AU - Chang, J.
AU - Thürmel, K.
AU - Roos, M.
AU - von Eynatten, M.
AU - Sollinger, D.
AU - Lutz, J.
AU - Heemann, U.
PY - 2009/7
Y1 - 2009/7
N2 - Background: Cardiovascular disease is a major cause of death after kidney transplantation; thus, cardiovascular protection is a major concern in transplant recipients. Data about cardiac characteristics from animal models after kidney transplantation are lacking. Therefore, we investigated cardiac structure and function in a model of chronic allograft injury. Methods: Kidneys from Fisher 344 rats were orthotopically transplanted into Lewis rats. Eight recipient rats were treated with placebo or an angiotensin II type-1 receptor blocker (AT1RB; candesartan cilexitil, 5 mg/kg/d) for 24 weeks posttransplantation, and 8 untreated matched Lewis rats were used as healthy controls. Echocardiography was performed at 24 weeks posttransplantation to measure ejection fraction, fractional shortening, and left ventricular mass, in triplicate. Proteinuria at 24 hours was determined, and after harvesting, the heart weight-body weight ratio (HW/BW) was measured. Results: At 24 weeks posttransplantation, renal transplant-recipient rats demonstrated a significantly decreased ejection fraction (mean [SD], 58.9% [3.2%] vs 70.7% [2.1%]) and fractional shortening (29.8% [2.0%] vs 38.3% [2.0%]) and increased HW/BW and left ventricular mass (7.7 [0.2] cm3 vs 6.7 [0.2] cm3) compared with healthy control rats. The HW/BW and left ventricular mass were significantly ameliorated by AT1RB compared with placebo-treated transplant-recipient rats (6.8 [0.2] cm3 vs 7.7 [0.2] cm3). In addition, decreased proteinuria was evident after AT1RB. Conclusion: The Fisher-Lewis rat kidney transplantation model resulted in cardiac hypertrophy and decreased cardiac function. AT1RB normalized cardiac hypertrophy without improving function. These findings demonstrate that the Fisher-Lewis rat renal transplantation model can be used to investigate transplantation-induced cardiomyopathy.
AB - Background: Cardiovascular disease is a major cause of death after kidney transplantation; thus, cardiovascular protection is a major concern in transplant recipients. Data about cardiac characteristics from animal models after kidney transplantation are lacking. Therefore, we investigated cardiac structure and function in a model of chronic allograft injury. Methods: Kidneys from Fisher 344 rats were orthotopically transplanted into Lewis rats. Eight recipient rats were treated with placebo or an angiotensin II type-1 receptor blocker (AT1RB; candesartan cilexitil, 5 mg/kg/d) for 24 weeks posttransplantation, and 8 untreated matched Lewis rats were used as healthy controls. Echocardiography was performed at 24 weeks posttransplantation to measure ejection fraction, fractional shortening, and left ventricular mass, in triplicate. Proteinuria at 24 hours was determined, and after harvesting, the heart weight-body weight ratio (HW/BW) was measured. Results: At 24 weeks posttransplantation, renal transplant-recipient rats demonstrated a significantly decreased ejection fraction (mean [SD], 58.9% [3.2%] vs 70.7% [2.1%]) and fractional shortening (29.8% [2.0%] vs 38.3% [2.0%]) and increased HW/BW and left ventricular mass (7.7 [0.2] cm3 vs 6.7 [0.2] cm3) compared with healthy control rats. The HW/BW and left ventricular mass were significantly ameliorated by AT1RB compared with placebo-treated transplant-recipient rats (6.8 [0.2] cm3 vs 7.7 [0.2] cm3). In addition, decreased proteinuria was evident after AT1RB. Conclusion: The Fisher-Lewis rat kidney transplantation model resulted in cardiac hypertrophy and decreased cardiac function. AT1RB normalized cardiac hypertrophy without improving function. These findings demonstrate that the Fisher-Lewis rat renal transplantation model can be used to investigate transplantation-induced cardiomyopathy.
UR - http://www.scopus.com/inward/record.url?scp=68949217033&partnerID=8YFLogxK
U2 - 10.1016/j.transproceed.2009.06.112
DO - 10.1016/j.transproceed.2009.06.112
M3 - Article
C2 - 19715985
AN - SCOPUS:68949217033
SN - 0041-1345
VL - 41
SP - 2612
EP - 2615
JO - Transplantation Proceedings
JF - Transplantation Proceedings
IS - 6
ER -
