Shivalkar B, Van Loon J, Wieland W, Tjandra-Maga T B, Borgers M, Plets C, Flameng W
Department of Cardiac Surgery, Katholieke Universiteit Leuven, Belgium.
Circulation. 1993 Jan;87(1):230-9. doi: 10.1161/01.cir.87.1.230.
Studies done in potential donors for heart transplantation and in experimental animals have suggested that brain death can have major histopathological and functional effects on the myocardium.
We developed experimental models of brain death using dogs to study the hemodynamic and catecholamine changes, the extent of myocardial structural damage, and the recovery potential of donor hearts obtained from brain-dead donors. Brain death was caused by increasing the intracranial pressure (ICP) suddenly or gradually by injecting saline in an epidural Foley catheter. In a first series of experiments, dogs given a sudden rise in ICP (n = 5) showed a hyperdynamic response and a 1,000-fold increase in the level of epinephrine after brain death. Histology revealed 93 +/- 2% of the myocardium to be severely ischemic. Dogs given a gradual rise in ICP (n = 6) showed a lesser hyperdynamic response, almost 200-fold increase in the level of epinephrine after brain death, and mild ischemic damage to the myocardium (23 +/- 1%). In a second series, hearts obtained from brain-dead and non-brain-dead donors were transplanted in recipients, and the weaning and recovery potential were studied. All four recipients with hearts from non-brain-dead donors were weaned with good functional recovery. Also, all four recipients with hearts from brain-dead dogs given a gradual rise in ICP were weaned with only moderate functional recovery. However, only two of four recipients with hearts from donors given a sudden rise in ICP were weaned and showed poor functional recovery.
Our results indicate that a sudden rise in ICP can cause irreversible myocardial damage.
对心脏移植潜在供体及实验动物的研究表明，脑死亡可对心肌产生重大组织病理学和功能影响。
我们利用犬类建立脑死亡实验模型，以研究血流动力学和儿茶酚胺变化、心肌结构损伤程度以及从脑死亡供体获取的供心的恢复潜力。通过向硬膜外Foley导管注射生理盐水突然或逐渐升高颅内压（ICP）来诱导脑死亡。在第一组实验中，颅内压突然升高的犬（n = 5）在脑死亡后表现出高动力反应，肾上腺素水平升高1000倍。组织学检查显示93±2%的心肌严重缺血。颅内压逐渐升高的犬（n = 6）表现出较小的高动力反应，脑死亡后肾上腺素水平升高近200倍，心肌有轻度缺血损伤（23±1%）。在第二组实验中，将脑死亡和非脑死亡供体的心脏移植到受体中，研究脱机和恢复潜力。所有接受非脑死亡供体心脏的四名受体均成功脱机，功能恢复良好。同样，所有接受颅内压逐渐升高的脑死亡犬心脏的四名受体均成功脱机，但功能恢复一般。然而，接受颅内压突然升高的供体心脏的四名受体中，只有两名成功脱机，且功能恢复较差。
我们的结果表明，颅内压突然升高可导致不可逆的心肌损伤。
