Bittner H B, Kendall S W, Campbell K A, Montine T J, Van Trigt P
Department of General and Cardiothoracic Surgery, Duke University Medical Center, Durham, NC 27710, USA.
J Heart Lung Transplant. 1995 Mar-Apr;14(2):308-17.
This study was designed to establish a validated canine brain death model. Ten consecutive dogs were studied to investigate the effects of brain death on hemodynamic, metabolic, and hormonal function.
Brain death was induced by inflation of a subdurally placed balloon and was validated neuropathologically. Functional data and blood samples were collected before and 15, 45, 90, 240, 360, and 420 minutes after the induction of brain death. No inotropic or vasoactive support was given. The results are expressed as mean +/- standard error of the mean.
The Cushing reflex occurred in all animals and lasted 13.3 +/- 1.5 minutes. Raised catecholamine levels were documented at 15 minutes, whereas the pituitary gland hormones vasopressin and adrenocorticotrophic hormone decreased significantly after 15 and 45 minutes, respectively. Triiodothyronine, thyroxine, and glucagon decreased significantly from 0.58 +/- 0.05 ng/ml, 2.20 +/- 0.15 micrograms/dl, and 49.7 +/- 9.1 pg/ml to 0.34 +/- 0.03 ng/ml (p < 0.05 versus baseline; paired two-tailed t-test), 1.14 +/- 1.14 micrograms/dl (p < 0.05), and 6.9 +/- 1.4 pg/ml (p < 0.05). Insulin and lactate dehydrogenase showed a moderate increase after brain death. Diabetes insipidus occurred after 45 minutes in nine animals (urine output 13.5 +/- 1.8 ml/kg/hour). Left and right ventricular end-diastolic pressure increased significantly toward the end of all experiments. Cardiac output increased and systemic and pulmonary vascular resistance decreased, but heart rate remained unchanged.
This simple, reproducible, moderately invasive, and reliable model of brain death in animals assesses donor organ function and preservation. Cushing reflex, hyperdynamic state, catecholamine storm, vasopressin and adrenocorticotropic hormone cessation, total cerebral necrosis, and diabetes insipidus were consistent findings.
本研究旨在建立一个经过验证的犬脑死亡模型。连续对10只犬进行研究，以探讨脑死亡对血流动力学、代谢和激素功能的影响。
通过向硬脑膜下放置的球囊充气诱导脑死亡，并通过神经病理学验证。在诱导脑死亡前以及诱导后15、45、90、240、360和420分钟收集功能数据和血样。未给予任何强心或血管活性支持。结果以平均值±平均标准误差表示。
所有动物均出现库欣反射，持续13.3±1.5分钟。15分钟时记录到儿茶酚胺水平升高，而垂体激素血管加压素和促肾上腺皮质激素分别在15分钟和45分钟后显著下降。三碘甲状腺原氨酸、甲状腺素和胰高血糖素从0.58±0.05 ng/ml、2.20±0.15 μg/dl和49.7±9.1 pg/ml显著降至0.34±0.03 ng/ml（与基线相比，p<0.05；配对双尾t检验）、1.14±1.14 μg/dl（p<0.05）和6.9±1.4 pg/ml（p<0.05）。脑死亡后胰岛素和乳酸脱氢酶有中度升高。9只动物在45分钟后出现尿崩症（尿量为13.5±1.8 ml/kg/小时）。在所有实验接近尾声时，左、右心室舒张末期压力显著升高。心输出量增加，全身和肺血管阻力降低，但心率保持不变。
这种简单、可重复、侵入性适中且可靠的动物脑死亡模型可评估供体器官功能及保存情况。库欣反射、高动力状态、儿茶酚胺风暴、血管加压素和促肾上腺皮质激素停止分泌、全脑坏死以及尿崩症是一致的发现。
