Der einfluss des hirntodes auf die freisetzung der atrialen und B-typ natriuretischen peptide und kardialen troponine in einem herzspendermodell

Atrium and brain natriuretic peptide (ANP and BNP) are secreted in the heart in response to pressure or volume overload and are sensitive and specific markers for severity of heart failure. Therefore, both markers may be used in the quality assessment of donor hearts. Cardiac troponins were shown to be predictors for early graft failure after HTx. However, the hemodynamic changes (Cushing reflex) due to brain death (BD) may affect levels of natriuretic peptides and cardiac troponins in heart donors. This study evaluated the effects of BD on the release of ANP, BNP, big endothelin 1 (big ET 1) and cardiac troponins in an animal model. After anesthesia and the initiation of monitoring, ten pigs were randomized into a BD group (n = 5) and a control group (n = 5). BD was induced by inflation of a subdurally positioned balloon catheter and anesthesia was stopped. In the control animals sham operation was performed and anesthesia was continued. Hemodynamics and BNP, ANP and big ET 1 plasma levels and cardiac troponin 1 and T (cTn1 and cTnT) serum levels were measured before and up to 13 hours after operation. Statistical analysis of the changes over time was performed using the Friedman test. The BD group presented significant increase of preload, afterload and cardiac output due to the Cushing reflex. In the control group the BNP level was higher than in the BD group and decreased over time (p=0.016). There was no significant change in BNP release in the BD group up to 13 hours after BD (p=0.1). ANP release remained stable over time in the control group (p=0.35) but decreased in the BD group (p=0.043). The big ET 1 levels were not different between groups and there were no changes over the time. cTnI was slightly elevated in the BD group 5 hours after BD (p<0.05), but remained under 1.5 mg/l throughout the study. cTnT was undetectable in both groups. Hemodynamic stress after BD did not lead to an increase of BNP and ANP levels. Moreover, brain function seems to influence the release of BNP and ANP from the myocardium. Further clinical evaluation of prognostic values of BNP and ANP levels for assessment of the quality of donor hearts is necessary. Cardiac troponins are a useful additional tool in the evaluation of donor heart quality.