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首页> 外文期刊>Journal of Neuroscience Methods >Characterization of a 3-vessel occlusion model for the induction of complete global cerebral ischemia in mice.
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Characterization of a 3-vessel occlusion model for the induction of complete global cerebral ischemia in mice.

机译：诱导小鼠完全性脑缺血的3血管闭塞模型的表征。

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摘要

Existing murine models of global cerebral ischemia are technically challenging thereby hampering the use of genetically engineered mice to study cardiac arrest-induced brain damage. We therefore investigated, if disconnecting the cerebral circulation from vertebral collateral blood flow by proximal occlusion of the basilar artery together with temporary bilateral common carotid artery occlusion (BCCAo) may be a more feasible approach. C57/Bl6 mice were anesthetized and the basilar artery was occluded through a ventral approach. Ten days later BCCAo was performed for 8-14min. Increasing durations of ischemia resulted in enhanced neuronal cell death in cortex, striatum, and hippocampus (22-63%) and increased neurological dysfunction and mortality (0-36%). Following 10min of BCCAo, the duration of global ischemia with the most favorable mortalityeuronal cell death ratio, hippocampal damage started 6h after the insult while cortical and striatal damage was delayed by at least 24h. No further loss of neuronal cells was observed later than 3 days. The proposed two-step approach resulted in complete cerebral ischemia and caused neuronal damage with high reproducibility and small variability. In combination with transgenic and knock-out mice this technically feasible model may help to extend our knowledge on the pathophysiology of cardiac arrest-induced brain damage.
机译：现有的全球脑缺血的鼠模型在技术上具有挑战性，从而阻碍了使用基因工程小鼠研究心脏骤停引起的脑损伤。因此，我们进行了调查，如果通过基底动脉近端闭塞以及暂时性双侧颈总颈动脉闭塞（BCCAo）断开大脑循环与椎侧支血流的联系可能是一种更可行的方法。麻醉C57 / B16小鼠，并通过腹侧入路阻塞基底动脉。十天后，BCCAo进行了8-14分钟。缺血持续时间的增加导致皮质，纹状体和海马中神经元细胞死亡的增加（22-63％），神经系统功能障碍和死亡率增加（0-36％）。 BCCAo 10分钟后，即整体缺血持续时间以最有利的死亡率/神经元细胞死亡比持续，在受伤后6h开始海马损伤，而皮层和纹状体损伤至少延迟了24h。 3天后未观察到神经元细胞的进一步损失。所提出的两步法可导致完全的脑缺血，并引起神经元损伤，其再现性高且变异性小。结合转基因和基因敲除小鼠，这种技术上可行的模型可能有助于扩展我们对心脏骤停诱发的脑损伤的病理生理学的认识。

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