Multiple sclerosis drugs: Sticker shock
Multiple sclerosis drugs: Sticker shock
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多发性硬化症药物：贴纸休克
DOI：
10.1002/ana.23608
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发表时间：
2012
影响因子：
11.2
通讯作者：
S. Johnston
中科院分区：
文献类型：
--
作者：
S. Hauser;S. Johnston
本研究探讨了短暂性双侧前脑缺血大鼠模型的四血管闭塞缺血性神经元损伤的时间分布。Wistar大鼠进行短暂的，但严重的前脑缺血永久闭塞椎动脉和24小时后暂时闭塞颈总动脉10，20或30分钟。颈动脉血流恢复，并在3、6、24和72小时后通过灌注固定处死大鼠。丢弃出现缺血后惊厥的大鼠。根据常规神经病理学标准对缺血性神经元损伤进行分级。四血管闭塞10分钟，在大多数大鼠的大脑半球中产生分散的缺血细胞改变。可见的神经元损伤的发作时间在脑区域之间变化，并且在一些区域中随着时间的推移而逐渐恶化。缺血30分钟后，小到中等大小的纹状体神经元早期受损，而海马h1区神经元可见损伤的开始延迟3到6小时。在24和72小时之间，新皮层（第3层、第5层和第6层，或两者）和海马（h1、h35、旁正中带）中受损的神经元数量显著增加（p< 0.01）。缺血性细胞变化的独特延迟发作和其发生率在24至72小时之间的延长增加可能反映了先前死亡的神经元中缺血性变化的延迟出现或延迟的损伤，其在缺血后期间继续危害受损但存活的神经元。
This study examined the temporal profile of ischemic neuronal damage following transient bilateral forebrain ischemia in the rat model of four-vessel occlusion. Wistar rats were subjected to transient but severe forebrain ischemia by permanently occluding the vertebral arteries and 24 hours later temporarily occluding the common carotid arteries for 10, 20, or 30 minutes. Carotid artery blood flow was restored and the rats were killed by perfusion-fixation after 3, 6, 24, and 72 hours. Rats with postischemic convulsions were discarded. Ischemic neuronal damage was graded in accordance with conventional neuropathological criteria. Ten minutes of four-vessel occlusion produced scattered ischemic cell change in the cerebral hemispheres of most rats. The time to onset of visible neuronal damage varied among brain regions and in some regions progressively worsened with time. After 30 minutes of ischemia, small to medium-sized striatal neurons were damaged early while the initiation of visible damage to hippocampal neurons in the h1 zone was delayed for 3 to 6 hours. The number of damaged neurons in neocortex (layer 3, layers 5 and 6, or both) and hippocampus (h1, h35, paramedian zone) increased significantly (p< 0.01) between 24 and 72 hours. The unique delay in onset of ischemic cell change and the protracte increase in its incidence between 24 and 72 hours could reflect either delayed-appearance of ischemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.