Detrimental effects of halothane narcosis on damage after endothelin-1-induced MCAO

Detrimental effects of halothane narcosis on damage after endothelin-1-induced MCAO
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DOI:
10.1016/j.jneumeth.2006.11.019
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发表时间:
2007-05-15
影响因子:
3
通讯作者:
Reymann, Klaus G.
Reymann, Klaus G.
中科院分区:
医学4区
文献类型:
--
作者:
Baldauf, Kathrin;Henrich-Noack, Petra;Reymann, Klaus G.

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麻醉在实验性中风研究中的影响是有争议的。我们使用内皮素-1诱导的大脑中动脉闭塞(eMCAO)模型来解决这个问题。该模型提供了比较在eMCAO诱导期间处于氟烷麻醉下的大鼠的梗死体积与在eMCAO期间没有麻醉的大鼠的病变的机会。所有动物均植入引导插管,可在自由活动的动物中诱导缺血。为了比较,一组动物在诱导缺血期间暴露于氟烷。eMCAO后7天,氟烷麻醉大鼠的平均梗死体积明显大于自由活动动物的病变。这种差异主要是由于皮质损伤增加,而纹状体的影响要小得多。与麻醉下eMCAO后7天的梗死体积相比,麻醉下诱导eMCAO后21天的皮质梗死体积显著减少。我们的研究结果表明,氟烷麻醉在eMCAO可以引起短暂的皮质增加缺血性梗死体积。在临床前测试潜在的神经保护药物用于临床应用时,应考虑挥发性麻醉剂对缺血病理生理学的影响。(C)2006 Elsevier B. V.保留所有权利。
The influence of anaesthesia in experimental stroke research is controversial. We addressed this problem using the model of endothelin-1-induced occlusion of the middle cerebral artery (eMCAO). This model provided the opportunity to compare the infarct volumes of rats which were under halothane anaesthesia during eMCAO induction with the lesions of rats which were without anaesthesia during eMCAO. All animals were implanted with guide cannulae which allowed the induction of ischaemia in freely moving animals. For comparison, one group of animals was exposed to halothane during the induction of ischaemia. Seven days after eMCAO, the average infarct volume of halothane-anaesthetised rats was significantly larger than the lesion in freely moving animals. This difference was mainly due to increased cortical damage, whereas the striatum was much less influenced. The cortical infarct volume 21 days after induction of eMCAO under anaesthesia was significantly reduced compared to the infarct volume 7 days after eMCAO under anaesthesia. Our results indicate that halothane anaesthesia during eMCAO can cause a transient cortical increase in ischaemic infarct volume. The influence of volatile anaesthetics on ischaemic pathophysiology should be taken into consideration when preclinically testing potential neuroprotective drugs for clinical applications. (C) 2006 Elsevier B.V. All rights reserved.