Prevention of myocardial injury during brain death by total cardiac sympathectomy in the Chacma baboon.
In a previous study, structural myocardial damage was found to occur in 60% of baboons after brain death had been induced by a rapid increase in intracranial pressure. In the present study, we attempt to clarify the causative mechanisms involved in the development of such injury. Three groups of baboons were subjected to brain death: group A, the control; group B, those with previous surgical or pharmacological cardiac sympathectomy or cardiac denervation; and group C, those with bilateral vagotomy, incomplete sympathectomy, or bilateral adrenalectomy. Electrocardiographic and hemodynamic responses to brain death were greatly modified in group B baboons compared with responses in groups A and C. Groups A and C showed a high incidence of myocardial necrosis, whereas no myocyte damage was seen in the hearts of group B baboons. The histological appearance of innervated hearts following brain death (groups A and C) may closely resemble that seen during an acute rejection episode following cardiac transplantation. We suggest that myocardial damage occurring during the process of dying may be related to endogenous catecholamine release (possibly resulting in increased calcium uptake by the myocardial cells), inducing various forms of myocyte necrosis. This may result in early failure in a donor heart following cardiac transplantation.
D
D
Novitzky
W N
WN
Wicomb
D K
DK
Cooper
A G
AG
Rose
B
B
Reichart
D000818:Animals; D001926:Brain Death; D009202:Cardiomyopathies / Q000097:blood / Q000209:etiology* / Q000473:pathology; D004562:Electrocardiography; D006321:Heart / Q000294:innervation*; D006439:Hemodynamics; D010215:Papio / Q000502:physiology*; D013562:Sympathectomy; D014628:Vagotomy