Donor preconditioning after the onset of brain death with dopamine derivate n-octanoyl dopamine improves early posttransplant graft function in the rat
Heart transplantation is the therapy of choice for end-stage heart failure. However, hemodynamic instability, which has been demonstrated in brain-dead donors (BDD), could also affect the posttransplant graft function. We tested the hypothesis that treatment of the BDD with the dopamine derivate n-o...
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| Hauptverfasser: | , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
24 January 2017
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| In: |
American journal of transplantation
Year: 2017, Jahrgang: 17, Heft: 7, Pages: 1802-1812 |
| ISSN: | 1600-6143 |
| DOI: | 10.1111/ajt.14207 |
| Online-Zugang: | Verlag, Volltext: http://dx.doi.org/10.1111/ajt.14207 Verlag, Volltext: https://onlinelibrary-wiley-com.ezproxy.medma.uni-heidelberg.de/doi/abs/10.1111/ajt.14207 
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| Verfasserangaben: | S. Li, S. Korkmaz-Icöz, T. Radovits, M. Ruppert, R. Spindler, S. Loganathan, P. Hegedűs, P. Brlecic, B. Theisinger, S. Theisinger, S. Höger, M. Brune, F. Lasitschka, M. Karck, B. Yard and G. Szabó |
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| 245 | 1 | 0 | |a Donor preconditioning after the onset of brain death with dopamine derivate n-octanoyl dopamine improves early posttransplant graft function in the rat |c S. Li, S. Korkmaz-Icöz, T. Radovits, M. Ruppert, R. Spindler, S. Loganathan, P. Hegedűs, P. Brlecic, B. Theisinger, S. Theisinger, S. Höger, M. Brune, F. Lasitschka, M. Karck, B. Yard and G. Szabó |
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| 520 | |a Heart transplantation is the therapy of choice for end-stage heart failure. However, hemodynamic instability, which has been demonstrated in brain-dead donors (BDD), could also affect the posttransplant graft function. We tested the hypothesis that treatment of the BDD with the dopamine derivate n-octanoyl-dopamine (NOD) improves donor cardiac and graft function after transplantation. Donor rats were given a continuous intravenous infusion of either NOD (0.882 mg/kg/h, BDD+NOD, n = 6) or a physiological saline vehicle (BDD, n = 9) for 5 h after the induction of brain death by inflation of a subdural balloon catheter. Controls were sham-operated (n = 9). In BDD, decreased left-ventricular contractility (ejection fraction; maximum rate of rise of left-ventricular pressure; preload recruitable stroke work), relaxation (maximum rate of fall of left-ventricular pressure; Tau), and increased end-diastolic stiffness were significantly improved after the NOD treatment. Following the transplantation, the NOD-treatment of BDD improved impaired systolic function and ventricular relaxation. Additionally, after transplantation increased interleukin-6, tumor necrosis factor TNF-α, NF-kappaB-p65, and nuclear factor (NF)-kappaB-p105 gene expression, and increased caspase-3, TNF-α and NF-kappaB protein expression could be significantly downregulated by the NOD treatment compared to BDD. BDD postconditioning with NOD through downregulation of the pro-apoptotic factor caspase-3, pro-inflammatory cytokines, and NF-kappaB may protect the heart against the myocardial injuries associated with brain death and ischemia/reperfusion. | ||
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