Prevention of Myocardial Injury During Brain Death by Total Cardiac Sympathectomy in the Chacma Baboon

Brain death and its implications for management of the potential organ donor

“…Myocardial damage and morphological changes following brain death are quite similar to changes that can be induced by high doses of catecholeamine infusion, 9 and they can be prevented by a total cardiac sympathectomy before the cerebral insult, indicating a substantial role of catecholeamines in triggering the myocardial injury following brain death. 10,11 Both the magnitude of the catecholeamine response and the extent of the myocardial injury seem to be correlated to the velocity of increase in ICP. In a dog model, an explosive increase in ICP resulted in a 750-fold increase in epinephrine and a 400-fold increase in norepinephrine plasma levels accompanied by extensive ischemic injury to the myocardium.…”

“…Most of the discussion is about catecholamines and their anticipated detrimental effects on the donor heart. Very high doses of catecholamines administered to experimental animals have induced damage to the myocardium similar to the changes induced by the sympathetic storm during brain death, [9][10][11] and the use of norepinephrine to donors has been related to primary nonfunction in heart transplantation. 87 This has led to high numbers of donors refused by cardiac surgeons exclusively due to the doses of catecholamines used.…”

Takotsubo Cardiomyopathy during Acute Adrenal Crisis due to Isolated Adrenocorticotropin Deficiency

“…She was critically ill and undoubtedly had intense activation of the sympathetic nervous system. Experimentally, brain-mediated cardiac injury can be prevented by total cardiac sympathectomy (30). Pharmacologic sympathetic blockade with propranolol and phentolamine also prevents myocardial necrosis after subarachnoid hemorrhage (31).…”

Electrocardiographic Score as a Predictor of Mortality After Subarachnoid Hemorrhage

“…The link between a high ECG score and mortality is not clear. The association of ECG changes with SAH has been attributed to the adverse effects of elevated concentrations of catecholamines [20][21][22][23][24][25][26][27][28] because the hemorrhage commonly involves the basilar cisterns, which are in close proximity to the hypothalamus, leading to excessive secretion of catecholamines. 20,21 At the cellular level, this causes hypermetabolism and electrolyte disturbances in the mitochondria and the subsequent ECG changes are the electrical expression of the intracellular/extracellular ion-balance modifications.…”

“…22 Furthermore, increased catecholamine release may lead to myocardial damage by direct toxicity. 23,24 NeilDwyer et al 29 investigated the relationship between plasma catecholamine concentrations and ECG abnormalities after SAH, and reported that catecholamines were above the normal range in patients with abnormal ECG findings. We did not investigate the role of catecholamines and their relation to the ECG abnormalities remains to be elucidated.…”