The pathophysiological effects of brain death on potential donor organs, with particular reference to the heart.
Major electrocardiographic, haemodynamic, and histopathological changes take place during the development of brain death; myocardial and pulmonary injury may result. Significant depletion of certain circulating hormones occurs, resulting in an inhibition of mitochondrial function, leading to reduced aerobic metabolic oxidative processes, affecting the body as a whole. Major organ energy stores are therefore diminished, leading to deterioration of function. Replacement of the depleted hormones, in particular triiodothyronine (T3), cortisol, and insulin, leads to rapid replacement of organ energy stores, associated with a return to normal function. T3 alone leads to reactivation of the mitochondria, stimulating aerobic metabolism. Hormonal therapy to brain-dead potential organ donors has been shown to lead to metabolic and haemodynamic stability, resulting in no wastage of organs, and in improved function after transplantation.
Cooper
D K
DK
Department of Cardiothoracic Surgery, Groote Schuur Hospital, Cape Town, South Africa.
Novitzky
D
D
Wicomb
W N
WN
D000818:Animals; D001926:Brain Death; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D006728:Hormones / Q000097:blood; D006801:Humans; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D010215:Papio; D013552:Swine; D014019:Tissue Donors; D014284:Triiodothyronine / Q000494:pharmacology
D006728:Hormones; D014284:Triiodothyronine