Donor preconditioning after the onset of brain death with dopamine derivate n-octanoyl dopamine improves early posttransplant graft function in the rat

• Verfasst von: Li, Shiliang [VerfasserIn]
• Verfasst von: Korkmaz-İçöz, Sevil [VerfasserIn]
• Verfasst von: Ruppert, Mihály [VerfasserIn]
• Verfasst von: Loganathan, Sivakkanan [VerfasserIn]
• Verfasst von: Hegedűs, Péter [VerfasserIn]
• Verfasst von: Höger, Simone [VerfasserIn]
• Verfasst von: Brune, Maik [VerfasserIn]
• Verfasst von: Lasitschka, Felix [VerfasserIn]
• Verfasst von: Karck, Matthias [VerfasserIn]
• Verfasst von: Yard, Benito A. [VerfasserIn]
• Verfasst von: Szabó, Gábor [VerfasserIn]
• Titel: Donor preconditioning after the onset of brain death with dopamine derivate n-octanoyl dopamine improves early posttransplant graft function in the rat
• Verf.angabe: 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
• E-Jahr: 2017
• Jahr: 24 January 2017
• Umfang: 11 S.
• Fussnoten: Gesehen am 20.07.2018 ; First published: 24 January 2017
• Titel Quelle: Enthalten in: American journal of transplantation
• Ort Quelle: [Amsterdam] : Elsevier, 2001
• Jahr Quelle: 2017
• Band/Heft Quelle: 17(2017), 7, Seite 1802-1812
• ISSN Quelle: 1600-6143
• DOI: doi:10.1111/ajt.14207
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: animal models
• Sach-SW: basic (laboratory) research/science
• Sach-SW: donors and donation: donation after brain death (DBD)
• Sach-SW: heart (allograft) function/dysfunction
• Sach-SW: heart transplantation/cardiology
• K10plus-PPN: 1577796543

Abstract

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.