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发育中小沙鼠对脑缺血的耐受性

Resistance to cerebral ischemia in developing gerbils.

作者信息

Kusumoto M, Arai H, Mori K, Sato K

机构信息

Department of Neurosurgery, Juntendo University, Tokyo, Japan.

出版信息

J Cereb Blood Flow Metab. 1995 Sep;15(5):886-91. doi: 10.1038/jcbfm.1995.110.

DOI:10.1038/jcbfm.1995.110
PMID:7673382
Abstract

Two-, three-, four-, five-, and twelve-week-old gerbils were subjected to various periods of bilateral carotid occlusion (BCO). Rectal and cranial temperatures were maintained at 37 degrees C during BCO, and only rectal temperature was monitored for 30 min of reperfusion. Seven days after ischemia, animals were perfusion-fixed and the neuronal densities in the hippocampal CA1 subfields were counted. The extent of cerebral ischemia during BCO was evaluated with [14C]iodoantipyrine autoradiography. The rectal temperature spontaneously fell to 33-34 degrees C during reperfusion in 2-week-old gerbils, although animals over 3 weeks old presented postischemic hyperthermia. Two-week-old animals therefore were divided into three experimental groups: In one group (2-week-old group I) rectal temperature was not regulated during 30 min of reperfusion, while in the other two groups (2-week-old groups II and III) rectal temperature was regulated at 37 and 38 degrees C, respectively, during reperfusion. Five-minute BCO produced almost complete destruction of the CA1 neurons in 12-week-old animals. In contrast, most CA1 neurons survived 30 min of BCO in 2-week-old group I and 15 min of BCO in 2-week-old groups II and III. [14C]Iodoantipyrine autoradiography revealed that BCO produced severe forebrain ischemia in 2-week-old gerbils as well as in 12-week-old gerbils. These findings indicate that developing gerbils have a greater tolerance to cerebral ischemia and that such ischemic tolerance is not due to a collateral network between the vertebrobasilar and the carotid circulations previously reported to develop more abundantly in developing gerbils.

摘要

对2周龄、3周龄、4周龄、5周龄和12周龄的沙鼠进行不同时长的双侧颈动脉闭塞(BCO)处理。在BCO期间,将直肠温度和颅温维持在37摄氏度,再灌注30分钟期间仅监测直肠温度。缺血7天后,对动物进行灌注固定,并对海马CA1亚区的神经元密度进行计数。用[14C]碘安替比林放射自显影术评估BCO期间脑缺血的程度。在再灌注期间,2周龄沙鼠的直肠温度自发降至33 - 34摄氏度,而3周龄以上的动物则出现缺血后体温过高。因此,将2周龄的动物分为三个实验组:在一组(2周龄I组)中,再灌注30分钟期间不调节直肠温度,而在另外两组(2周龄II组和III组)中,再灌注期间分别将直肠温度调节至37摄氏度和38摄氏度。5分钟的BCO导致12周龄动物的CA1神经元几乎完全被破坏。相比之下,2周龄I组中大多数CA1神经元在30分钟的BCO后存活,2周龄II组和III组中在15分钟的BCO后存活。[14C]碘安替比林放射自显影术显示,BCO在2周龄沙鼠和12周龄沙鼠中均导致严重的前脑缺血。这些发现表明,发育中的沙鼠对脑缺血具有更大的耐受性,并且这种缺血耐受性并非由于先前报道的在发育中的沙鼠中更丰富地形成的椎基底动脉和颈动脉循环之间的侧支网络。

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