Bootcongres

Introduction: In contrast to other solid organ transplantations, the five year graft survival in lung transplantation remains inferior. Brain death leads to a systemic inflammatory release of pro-inflammatory mediators with a consecutive loss in barrier function in the lung, worsened by cold ischemia reperfusion injury after transplantation. Pre-conditioning therapy with dopamine in the brain dead donor has been successfully employed for prolonged graft survival in kidney and heart transplantation. To prevent undesired side effects of dopamine, the non-hemodynamic derivative N-octanoyl dopamine (NOD) was developed. Since NOD showed anti-inflammatory properties and a benefit in acute kidney injury, the aim of this study was to investigate if NOD can decrease acute inflammation and improve lung function in a model of brain dead donor lung transplantation. Methods: 24 Fischer rats were randomly assigned into three donor groups for isogenic left lung transplantation: 1) untreated control group, 2) acute traumatic brain death (BD) and 3) brain death with continuous NOD treatment. All animals were stabilized above a mean arterial pressure of 80mmHg by fluid resuscitation and ventilated for 4 hours before lung harvest. The recipient animals received a single lung transplantation and were ventilated for 6 hours after transplantation. Gas-exchange and respiratory system mechanics were analyzed. Results: Before lung transplantation there were no substantial differences between the three donor groups. However, after transplantation the oxygenation index is better in the control group compared to the brain death groups both 5 minutes and 6hrs. after reperfusion. Interestingly, the NoD treated lungs were the only ones that improved during the 6hrs. of ventilation. Soon, we hope to be able to show also an anti-inflammatory effect in the NOD treated lungs. Conclusion: In contrast to untreated donors, NOD therapy in the brain dead donor improves respiratory function in the transplanted lung.