Novitzky D, Wicomb W N, Cooper D K, Rose A G, Reichart B
Ann Thorac Surg. 1986 May;41(5):520-4. doi: 10.1016/s0003-4975(10)63032-9.
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.
在先前的一项研究中，发现通过快速升高颅内压诱导脑死亡后，60%的狒狒出现了心肌结构损伤。在本研究中，我们试图阐明这种损伤发生发展的致病机制。将三组狒狒诱导至脑死亡状态：A组为对照组；B组为先前接受过手术或药物性心脏交感神经切除术或心脏去神经支配的狒狒；C组为接受双侧迷走神经切断术、不完全交感神经切除术或双侧肾上腺切除术的狒狒。与A组和C组相比，B组狒狒对脑死亡的心电图和血流动力学反应有很大改变。A组和C组心肌坏死发生率较高，而B组狒狒心脏未观察到心肌细胞损伤。脑死亡后有神经支配的心脏（A组和C组）的组织学表现可能与心脏移植后急性排斥反应期间所见非常相似。我们认为，濒死过程中发生的心肌损伤可能与内源性儿茶酚胺释放有关（可能导致心肌细胞钙摄取增加），进而诱导各种形式的心肌细胞坏死。这可能导致心脏移植后供体心脏早期功能衰竭。
