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The pathophysiological effects of brain death on potential donor organs, with particular reference to the heart.

Abstract
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.
AuthorsD K Cooper, D Novitzky, W N Wicomb
JournalAnnals of the Royal College of Surgeons of England (Ann R Coll Surg Engl) Vol. 71 Issue 4 Pg. 261-6 (Jul 1989) ISSN: 0035-8843 [Print] England
PMID2774455 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Hormones
  • Triiodothyronine
Topics
  • Animals
  • Brain Death
  • Heart (physiopathology)
  • Hemodynamics
  • Hormones (blood)
  • Humans
  • Myocardium (metabolism)
  • Oxygen Consumption (drug effects)
  • Papio
  • Swine
  • Tissue Donors
  • Triiodothyronine (pharmacology)

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