Ischemic preconditioning in 18-to 20-month-old gerbils - Long-term survival with functional outcome measures
Ischemic preconditioning in 18-to 20-month-old gerbils - Long-term survival with functional outcome measures
复制标题
DOI：
10.1161/01.str.30.6.1240
复制
发表时间：
1999-06-01
期刊：
影响因子：
8.3
通讯作者：
Corbett, D
中科院分区：
文献类型：
--
作者：
Dowden, J;Corbett, D
背景和目的：在幼年动物中，缺血预处理可保护海马CA 1区神经元免受全脑缺血的影响。然而，脑缺血最常发生在年龄大于或等于65岁的个体中。本研究探讨了在人口中的老年人（18- 20个月大）沙鼠缺血预处理提供的保护。Methods-一组动物暴露于两个1.5分钟的全球缺血事件分开24小时，随后72小时后，由5分钟闭塞的两个颈动脉。第二组仅给予2次预处理。另外两组暴露于5分钟的缺血或假手术。动物存活10、30或60天。功能和组织学评估被用来确定程度的protection.Results-ten天后缺血有>80%的保护CA 1神经元在缺血预处理动物相比，在缺血沙鼠的6%。然而，这些预处理的动物在旷场习惯化测试中受损。此外，CA 1树突状场电位的幅度小于假手术动物。虽然有一个完全丧失的染色CA 1微管相关蛋白-2缺血动物，染色缺血预处理的动物是正常的。这表明树突异常本身并不是观察到的功能缺陷的原因。CA 1细胞存活率下降至接近假手术值的75%（P
Background and Purpose-In young animals, ischemic preconditioning protects CA1 hippocampal neurons against global ischemia. However, cerebral ischemia occurs most frequently in individuals aged greater than or equal to 65 years. This study examined the protection provided by ischemic preconditioning in a population of aged (18- to 20-month-old) gerbils.Methods-One group of animals was exposed to two 1.5-minute episodes of global ischemia separated by 24 hours and followed 72 hours later by a 5-minute occlusion of both carotid arteries. A second group was given 2 episodes of preconditioning only. Two other groups were exposed to 5 minutes of ischemia or sham surgery. The animals survived 10, 30, or 60 days. Functional and histological assessments were used to determine the extent of protection.Results-Ten days after ischemia there was >80% protection of CA1 neurons in ischemic preconditioned animals compared with 6% in ischemic gerbils. Nevertheless, these preconditioned animals were impaired in open-field tests of habituation. In addition, CA1 dendritic field potentials were smaller in amplitude compared with those in sham animals. While there was a complete loss of staining for CA1 microtubule-associated protein-2 in ischemic animals, staining in ischemic preconditioned animals was normal. This suggests that dendritic abnormalities per se were not responsible for the observed functional deficits. CA1 cell survival declined to approximate to 75% of sham values (P