Fink Ericka L, Marco Christina D, Donovan Holly A, Alexander Henry, Dixon C Edward, Jenkins Larry W, Stange Christopher J, Kochanek Patrick M, Clark Robert S B
Department of Critical Care Medicine, Safar Center for Resuscitation Research, Pittsburgh, PA, USA.
Dev Neurosci. 2005 Mar-Aug;27(2-4):191-9. doi: 10.1159/000085992.
The American Heart Association has endorsed the use of mild hypothermia for adults after cardiopulmonary arrest. However, there are no contemporary trials testing hypothermia in children after cardiopulmonary arrest and extrapolation from adult studies is problematic given differences in brain development and primary etiology (asphyxia in children vs. ventricular arrhythmia in adults). Accordingly, we tested the effects of mild postresuscitative hypothermia on functional and histopathological outcome after asphyxial cardiac arrest in juvenile rats. Postnatal day 17 rats were subjected to 8 min of asphyxia-induced cardiac arrest followed by resuscitation. Rats were randomized to normothermic (37 degrees C), hypothermic (32 degrees C), or unregulated temperature groups (n = 7-8/group) to begin after return of spontaneous circulation for a duration of 1 h. Brain temperature in the unregulated group dropped to 34.0 +/- 0.4 degrees C at 1 h. The hypothermic group had improved motor function assessed using beam balance and inclined plane tests vs. the normothermic group. The depth of hypothermia was associated with increased CA1 hippocampal neuron survival at 5 weeks. Neurodegeneration in the CA1 hippocampus assessed using Fluoro-Jade B labeling at 5 weeks was not detected in the 32 degrees C group, whereas 2/7 and 4/7 rats in the 34 and 37 degrees C groups, respectively, showed neurodegeneration. Brief treatment with moderate induced hypothermia improved functional outcome and prevented long-term neurodegeneration in a model that mimics the clinical and histopathological scenario of pediatric cardiac arrest. Similar to adults, infants and children may benefit from induced hypothermia after cardiopulmonary arrest, warranting further study.
美国心脏协会已认可在成人心肺复苏后使用轻度低温治疗。然而,目前尚无针对儿童心肺复苏后低温治疗的当代试验,鉴于大脑发育和主要病因的差异(儿童为窒息,成人为室性心律失常),从成人研究推断存在问题。因此,我们测试了轻度复苏后低温对幼年大鼠窒息性心脏骤停后功能和组织病理学结果的影响。出生后第17天的大鼠经历8分钟窒息诱导的心脏骤停,随后进行复苏。大鼠被随机分为常温组(37摄氏度)、低温组(32摄氏度)或温度未调控组(每组n = 7 - 8只),在自主循环恢复后开始,持续1小时。未调控组在1小时时脑温降至34.0±0.4摄氏度。与常温组相比,低温组使用平衡木和斜面试验评估的运动功能有所改善。低温深度与5周时海马CA1区神经元存活率增加相关。在5周时,使用Fluoro - Jade B标记评估,32摄氏度组未检测到海马CA1区神经退行性变,而34摄氏度组和37摄氏度组分别有2/7和4/7的大鼠出现神经退行性变。在一个模拟小儿心脏骤停临床和组织病理学情况的模型中,短暂的中度诱导低温治疗改善了功能结果并预防了长期神经退行性变。与成人相似,婴儿和儿童可能从心肺复苏后诱导低温治疗中获益,值得进一步研究。