TRANSIENT SPINAL ISCHEMIA IN THE RAT - CHARACTERIZATION OF BEHAVIORAL AND HISTOPATHOLOGICAL CONSEQUENCES AS A FUNCTION OF THE DURATION OF AORTIC OCCLUSION

TRANSIENT SPINAL ISCHEMIA IN THE RAT - CHARACTERIZATION OF BEHAVIORAL AND HISTOPATHOLOGICAL CONSEQUENCES AS A FUNCTION OF THE DURATION OF AORTIC OCCLUSION
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DOI:
10.1038/jcbfm.1994.65
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发表时间:
1994-05-01
影响因子:
6.3
通讯作者:
YAKSH, TL
YAKSH, TL
中科院分区:
医学1区
文献类型:
--
作者:
MARSALA, M;YAKSH, TL

文献摘要

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为了表征短暂缺血后脊髓中发生的行为和组织病理学变化,在氟烷(1-1. 5%)麻醉大鼠插入和随后的膨胀的2F Fogarty导管为10,15,20,或30分钟。神经恢复进行了测试,在8小时的再灌注。再流后,缺血30 min的动物在1 h时出现初始松弛,4 h时出现痉挛,8 h时出现松弛。缺血20分钟后,最初出现松弛,随后出现后肢痉挛,持续8小时。较短的缺血时间间隔对运动功能的影响最小。复流后,动物出现明显的异常性呼吸,其发生率取决于缺血的持续时间。组织病理学改变与神经功能缺损程度有明显相关性。在痉挛性动物中,位于第三至第七层的小型和中型中间神经元受到影响。动物在8小时的弛缓另外显示了显着的发生率嗜银A运动神经元的腹角。与异常性疼痛的频繁出现相对应,这些动物在第II层中也显示出大量受损的神经元。
To characterize the behavioral and histopathological changes that occur in spinal cord after transient ischemia, reversible occlusion of the descending aorta was achieved in the halothane (1-1. 5%)-anesthetized rat by the insertion and subsequent inflation of a 2F Fogarty catheter for 10, 15, 20, or 30 min. Neurological recovery was tested during 8 h of reperfusion. After reflow, animals undergoing 30 min of ischemia displayed an initial flaccidity at 1 h, spasticity at 4 h, and flaccidity at the end of 8 h. Following 20 min of ischemia the initial flaccidity was followed by hindlimb spasticity that persisted for 8 h. Shorter intervals of ischemia had minimal effects on motor function. After reflow, animals developed a prominent allodynea, the incidence of which was dependent on the duration of ischemia. A clear correlation of histopathological changes with the degree of neurological deficit was noted. In spastic animals, small and medium-sized interneurons localized in laminae III to VII were affected. Animals with flaccidity at 8 h additionally displayed a significant incidence of argyrophilic A motoneurons in the ventral horns. Corresponding to the frequent appearance of allodynea, these animals also showed a significant number of damaged neurons in lamina II.