Katz L, Ebmeyer U, Safar P, Radovsky A, Neumar R
Safar Center for Resuscitation Research, University of Pittsburgh Medical Center, Pennsylvania 15260, USA.
J Cereb Blood Flow Metab. 1995 Nov;15(6):1032-9. doi: 10.1038/jcbfm.1995.129.
An outcome model with asphyxial cardiac arrest in rats has been developed for quantifying brain damage. Twenty-two rats were randomized into three groups. Control group I was normal, was conscious, and had no asphyxia (n = 6). Sham group II had anesthesia and surgery but no asphyxia (n = 6). All 12 rats in groups I and II survived to 72 h and were functionally and histologically normal. Arrest group III (the model; n = 10) had light anesthesia and apneic asphyxia of 8 min, which led to cessation of circulation at 3-4 min of apnea, resulting in cardiac arrest (no flow) of 4-5 min. All 10 rats had spontaneous circulation restored by standard external cardiopulmonary resuscitation. Nine rats survived controlled ventilation for 1 h and observation to 72 h, while one rat died before extubation. All nine survivors were conscious at 72 h, with neurologic deficit scores (0% = best; 100% = worst) of 7 +/- 6% (2-16%). All brain regions at five coronal levels were examined for ischemic neurons. The prevalence of ischemic neurons in five regions was categorically scored. The average total brain histopathologic damage score in group III (n = 9) was 2.1 (p < 0.05 vs. group I or II). A reproducible outcome model of cardiac arrest in rats was documented. It provides a tool for investigating pathophysiological mechanisms of neuronal death caused by a transient global hypoxic-ischemic brain insult.
已建立一种用于量化脑损伤的大鼠窒息性心脏骤停结局模型。22只大鼠被随机分为三组。对照组I正常、清醒且无窒息(n = 6)。假手术组II接受麻醉和手术但无窒息(n = 6)。I组和II组的所有12只大鼠均存活至72小时,功能和组织学均正常。骤停组III(模型组;n = 10)接受轻度麻醉并进行8分钟的呼吸性窒息,在窒息3 - 4分钟时导致循环停止,进而引发4 - 5分钟的心脏骤停(无血流)。所有10只大鼠通过标准的体外心肺复苏恢复了自主循环。9只大鼠在控制通气1小时并观察至72小时后存活,而1只大鼠在拔管前死亡。所有9只存活大鼠在72小时时均清醒,神经功能缺损评分(0% = 最佳;100% = 最差)为7±6%(2 - 16%)。对五个冠状层面的所有脑区进行缺血神经元检查。对五个区域缺血神经元的患病率进行分类评分。III组(n = 9)的平均全脑组织病理学损伤评分为2.1(与I组或II组相比,p < 0.05)。记录了一种可重复的大鼠心脏骤停结局模型。它为研究短暂性全脑缺氧缺血性脑损伤导致神经元死亡的病理生理机制提供了一种工具。