Department of Neuroscience, Section of Neurosurgery, Uppsala University Hospital, Uppsala University, Uppsala, Sweden.
Crit Care Med. 2011 Mar;39(3):512-7. doi: 10.1097/CCM.0b013e318206b824.
Brain death impairs organ function and outcome after transplantation. There is a need for a brain death model to allow studies of organ viability and preservation. For neurointensive care research, it is also of interest to have a relevant brain death model for studies of intracranial dynamics and evaluation of cerebral monitoring devices. Therefore, the objective was to develop a standardized clinically relevant brain death model.
Six pigs of both sexes (10-12 wks old; mean weight, 24.5±1.4 kg) were included. Mean arterial blood pressure, heart rate, intracranial pressure, intracranial compliance, cerebral perfusion pressure, and brain tissue oxygenation (BtiPo2) were recorded during stepwise elevation of intracranial pressure by inflation of an epidural balloon catheter with saline (1 mL/20 mins). Brain death criteria were decided to be reached when cerebral perfusion pressure was <0 mm Hg for 60 mins and at least 10 mL saline was inflated epidurally. BtiPo2 and arterial injections of microspheres were used for confirmation of brain death.
A gradual volume-dependent elevation of intracranial pressure was observed. After 10 mL of balloon infusion, mean intracranial pressure was 89.8±9.7 (sd) mm Hg. Intracranial compliance decreased from 0.137±0.069 mL/mm Hg to 0.007±0.001 mL/mm Hg. The mean arterial pressure decreased and the heart rate increased when the intracranial volume was increased to between 5 and 6 mL. All animals showed cerebral perfusion pressure≤0 after 7 to 10 mL of infusion. In all animals, the criteria for brain death with negative cerebral perfusion pressure and BtiPo2 ∼0 mm Hg were achieved. Only a negligible amount of microspheres were found in the cerebrum, confirming brain death. The kidneys showed small foci of acute tubular necrosis.
The standardized brain death model designed in pigs simulates the clinical development of brain death in humans with a classic pressure-volume response and systemic cardiovascular reactions. Brain death was convincingly confirmed.
脑死亡会损害移植后的器官功能和预后。因此，需要建立脑死亡模型来研究器官活力和保存。对于神经重症监护研究，建立相关的脑死亡模型对于研究颅内动力学和评估脑监测设备也很有意义。因此，本研究旨在建立一种标准化的临床相关脑死亡模型。
本研究纳入了 6 头雌雄各半的猪（10-12 周龄；平均体重 24.5±1.4 kg）。通过向硬膜外球囊导管内注入盐水（1 mL/20 分钟）逐步升高颅内压，记录平均动脉血压、心率、颅内压、颅内顺应性、脑灌注压和脑组织氧合指数（BtiPo2）。当脑灌注压<0 mmHg 持续 60 分钟且硬膜外注入至少 10 mL 盐水时，即决定达到脑死亡标准。通过 BtiPo2 和动脉内微球注射来确认脑死亡。
观察到颅内压呈逐渐升高的容积依赖性。球囊输注 10 mL 后，平均颅内压为 89.8±9.7（标准差）mmHg。颅内顺应性从 0.137±0.069 mL/mm Hg 降至 0.007±0.001 mL/mm Hg。当颅内容量增加到 5-6 mL 之间时，平均动脉压下降，心率增加。所有动物在输注 7-10 mL 后均出现脑灌注压≤0。所有动物均达到了脑死亡的标准，即脑灌注压<0mmHg 且 BtiPo2≈0mmHg。仅在大脑中发现了少量的微球，证实了脑死亡。肾脏显示出少量的急性肾小管坏死。
本研究在猪中设计的标准化脑死亡模型模拟了人类脑死亡的临床发展过程，具有典型的压力-容积反应和全身心血管反应。脑死亡得到了令人信服的确认。
