Frick Tamara, Springe Dirk, Grandgirard Denis, Leib Stephen L, Haenggi Matthias
a Department of Intensive Care Medicine , University Hospital - Inselspital, University of Bern , Switzerland.
b Neuroinfection Laboratory, Institute for Infectious Diseases , University of Bern , Switzerland.
Neurol Res. 2016 Apr;38(4):373-80. doi: 10.1179/1743132815Y.0000000090. Epub 2016 Apr 20.
Cerebral hypoxic-ischaemic injury following cardiac arrest is a devastating disease affecting thousands of patients each year. There is a complex interaction between post-resuscitation injury after whole-body ischaemia-reperfusion and cerebral damage which cannot be explored in in vitro systems only; there is a need for animal models. In this study, we describe and evaluate the feasibility and efficiency of our simple rodent cardiac arrest model. >
Ten wistar rats were subjected to 9 and 10 minutes of cardiac arrest. Cardiac arrest was introduced with a mixture of the short-acting beta-blocking drug esmolol and potassium chloride.
All animals could be resuscitated within 1 minute, and survived until day 5. General health score and neurobehavioural testing indicated substantial impairment after cardiac arrest, without differences between groups. Histological examination of the hippocampus CA1 segment, the most vulnerable segment of the cerebrum, demonstrated extensive damage in the cresyl violet staining, as well as in the Fluoro-Jade B staining and in the Iba-1 staining, indicating recruitment of microglia after the hypoxic-ischaemic event. Again, there were no differences between the 9- and 10-minute cardiac arrest groups.
We were able to establish a simple and reproducible 9- and 10-minute rodent cardiac arrest model with a well-defined no-flow-time. Extensive damage can be found in the hippocampus CA1 segment. The lack of difference between 9- and 10-minute cardiac arrest time in the neuropsychological, the open field test and the histological evaluations is mainly due to the small sample size.
心脏骤停后的脑缺氧缺血性损伤是一种毁灭性疾病，每年影响数千名患者。全身缺血再灌注后的复苏后损伤与脑损伤之间存在复杂的相互作用，这无法仅在体外系统中进行探究；因此需要动物模型。在本研究中，我们描述并评估了我们简单的啮齿动物心脏骤停模型的可行性和效率。
对10只Wistar大鼠进行9分钟和10分钟的心脏骤停。使用短效β受体阻滞剂艾司洛尔和氯化钾的混合物诱导心脏骤停。
所有动物均能在1分钟内复苏，并存活至第5天。总体健康评分和神经行为测试表明心脏骤停后有明显损伤，两组之间无差异。对大脑最易受损的海马CA1段进行组织学检查，在甲酚紫染色、氟玉红B染色和Iba-1染色中均显示出广泛损伤，表明缺氧缺血事件后小胶质细胞被募集。同样，9分钟和10分钟心脏骤停组之间没有差异。
我们能够建立一个简单且可重复的9分钟和10分钟啮齿动物心脏骤停模型，其无血流时间明确。在海马CA1段可发现广泛损伤。9分钟和10分钟心脏骤停时间在神经心理学、旷场试验和组织学评估方面缺乏差异，主要是由于样本量小。
