Brain death and donor heart dysfunction: implications in cardiac transplantation.
OBJECTIVE
In this article, the hemodynamic, humoral, and immunological perturbations following brain death (BD) are going to be discussed in a stepwise manner.


METHODS
BD produces derangements in cardiac function, through a not-yet-well-explained mechanism. Using literature review, we attempted to delineate the "pathophysiology" involved.


RESULTS
A severe a-adrenergic stimulation following catecholamine storm results in conditions such that the pulmonary capillary pressure is massively increased. Furthermore, cytokine up-regulation, endothelial expression molecules, and neutrophil infiltration produce tissue damage. The end result reflects myocardial necrosis due to reduction of the calcium ATPase activity that leads to myocyte calcium overload and cell death.


CONCLUSIONS
Delineation of the mechanisms responsible for donor heart dysfunction (DHD) would be presented. Furthermore, an attempt would be made to apply this knowledge into the clinical practice in order to increase the suitability of donor hearts for transplantation.
Apostolakis
Efstratios
E
University of Patras Medical School, Patras, Greece.
Parissis
Haralambos
H
Dougenis
Dimitrios
D
D015415:Biomarkers; D001926:Brain Death; D002395:Catecholamines; D006331:Heart Diseases / Q000503:physiopathology*; D016027:Heart Transplantation / Q000592:standards*; D006801:Humans; D009206:Myocardium / Q000166:cytology / Q000473:pathology; D009336:Necrosis; D009926:Organ Preservation / Q000379:methods*; D011943:Receptors, Adrenergic, beta; D014019:Tissue Donors
D015415:Biomarkers; D002395:Catecholamines; D011943:Receptors, Adrenergic, beta