Biphasic response after brain death induction: prominent part of catecholamines release in this phenomenon

The Effects of Hormone Resuscitation on Cardiac Function and Hemodynamics in a Porcine Brain-Dead Organ Donor Model

“…Chiari et al reported a small increase in troponin I levels after brain death in pigs, consistent with myocardial ischemic injury (49). Troponin I levels recorded 3 h after brain death in their study were comparable to those recorded in our study, allowing for differences in assay techniques and in the degree of surgical preparation of the heart between Hormone Resuscitation in Donor Management the two studies.…”

“…This indicates the development of rapid desensitization to norepinephrine at the vascular level, which occurred in parallel with the myocardial desensitization described above. The cause for this vascular desensitization is unclear but could be explained by high circulating levels of endogenous catecholamines after brain death (37,49) acting directly on the a 1 -adrenergic receptor (51), or by the loss of other vasoconstrictor mechanisms after brain death (14,20,52). Regardless of the mechanism, our findings indicate that norepinephrine alone is a poor choice to maintain blood pressure in the brain dead donor.…”

Brain Death Effects on Catecholamine Levels and Subsequent Cardiac Damage Assessed in Organ Donors

“…These observations are consistent with the findings reported in animal models. 29,30 The release kinetics of the hormones established includes a peak at the moment of BD, with levels normalizing thereafter followed by a fall to below-normal levels. 31 A second peak was observed 45 minutes after BD in one study 32 and even several hours after death in another study.…”

Graft Immunogenicity Revisited: Relevance of Tissue-Specific Immunity, Brain Death and Donor Pretreatment

“…In addition, the authors found a significant correlation with rises in IL-6 and soluble TNF and IL-2 receptors as markers for the activation of immunological cascades. The release of large amounts of catecholamines immediately after the induction of brain death has also been observed in various animal models [39, 40]. Although a second peak of catecholamines may appear 120 min after the induction of brain death in pigs [40], we still have incomplete information on the profile of systemic catecholamine release during the time after brain death.…”

“…The release of large amounts of catecholamines immediately after the induction of brain death has also been observed in various animal models [39, 40]. Although a second peak of catecholamines may appear 120 min after the induction of brain death in pigs [40], we still have incomplete information on the profile of systemic catecholamine release during the time after brain death. Surprisingly, in a rabbit model of brain death, it was found that dopamine and norepinephrine impaired renal perfusion.…”