Hormonal changes in brain death and immune activation in the donor

Transpl Int. 2000;13 Suppl 1:S282-5. doi: 10.1007/s001470050342.


Kidneys obtained from brain dead donors show inferior graft survival compared to living donation. The effects of brain death itself are thought to be partly responsible for these results. We, therefore, examined levels of catecholamines, the vasoconstricting hormones AT II, ET-1 and renin activity, pituitary hormones, and their correlation to pro-inflammatory cytokines and cytokine receptors. In 17 brain dead patients and 19 preoperative neurosurgical patients, these parameters were measured by HPLC, RIA and ELISA. Brain death resulted in massive increases in serum catecholamines, AT II and ET-1, as well as PRA, whereas thyroid and adrenal hormone levels remained unchanged. We found a significant correlation with rises in IL-6 and soluble TNF and IL-2 receptors as markers for the activation of immunological cascades. We concluded that these effects could be directly and indirectly responsible for the impaired organ perfusion and function observed in brain death.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Angiotensin II / analysis
  • Antigens, CD / blood
  • Brain Death*
  • Cytokines / blood*
  • Endothelin-1 / blood
  • Epinephrine / blood
  • Female
  • Hormones / blood*
  • Humans
  • Interleukins / blood
  • Male
  • Middle Aged
  • Norepinephrine / blood
  • Pituitary Hormones / blood
  • Receptors, Cytokine / blood*
  • Receptors, Interleukin-2 / blood
  • Receptors, Tumor Necrosis Factor / blood
  • Receptors, Tumor Necrosis Factor, Type II
  • Renin / blood
  • Tissue Donors*


  • Antigens, CD
  • Cytokines
  • Endothelin-1
  • Hormones
  • Interleukins
  • Pituitary Hormones
  • Receptors, Cytokine
  • Receptors, Interleukin-2
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Type II
  • Angiotensin II
  • Renin
  • Norepinephrine
  • Epinephrine