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猫大脑中动脉闭塞相关的皮质缺血半暗带:2. 组织病理学、含水量及体外神经递质摄取研究

The cortical ischaemic penumbra associated with occlusion of the middle cerebral artery in the cat: 2. Studies of histopathology, water content, and in vitro neurotransmitter uptake.

作者信息

Strong A J, Tomlinson B E, Venables G S, Gibson G, Hardy J A

出版信息

J Cereb Blood Flow Metab. 1983 Mar;3(1):97-108. doi: 10.1038/jcbfm.1983.12.

Abstract

The nature of the ischaemic penumbra, as defined by suppression of electroencephalogram amplitude in the absence of increase in steady state pial surface potassium activity in excess of 13 mM, was examined in the marginal gyrus of cats subjected to middle cerebral artery occlusion. In vitro synaptosomal neurotransmitter uptake, water content (specific gravity), and histopathology at the light and electron microscopic level were studied and the results compared with those obtained at deeper, critical levels of ischaemia (less than 15 ml 100 g-1 min-1). [3H]4-Aminobutyric acid uptake was 104% of control in the marginal gyrus (NS), and 61 and 48% (p less than 0.05) in critical ischaemia. It is concluded that impairment of in vivo synaptosomal uptake is a marker of simultaneous widespread damage to neurones, rather than of a change restricted to the synaptic compartment, although the present findings cannot exclude reversible, substrate-limited impairment of uptake in vivo. Reductions in specific gravity were seen only with critical ischaemia. In 5 of 6 experiments, early or classical ischaemic neuronal cell changes and reactive glia were seen on light microscopy in restricted areas in the marginal gyrus, either in microfoci or scattered more diffusely. Ultrastructural changes were more frequent but were considered to affect only a minority of neurones. Hypotheses for selective electrophysiological suppression in penumbra are discussed.

摘要

在大脑中动脉闭塞的猫的边缘回中,研究了缺血半暗带的性质,其定义为在稳态软脑膜表面钾活性不超过13 mM增加的情况下脑电图振幅的抑制。研究了体外突触体神经递质摄取、含水量(比重)以及光镜和电镜水平的组织病理学,并将结果与在更深的、临界缺血水平(小于15 ml 100 g-1 min-1)获得的结果进行比较。边缘回中[3H]4-氨基丁酸摄取为对照的104%(无统计学意义),在临界缺血时为61%和48%(p<0.05)。得出的结论是,体内突触体摄取受损是神经元同时广泛受损的标志,而不是仅限于突触区室的变化,尽管目前的研究结果不能排除体内摄取存在可逆的、底物限制的损伤。仅在临界缺血时观察到比重降低。在6个实验中的5个中,在边缘回的受限区域,无论是微灶还是更弥漫地散在分布,在光镜下都观察到早期或典型的缺血性神经元细胞变化和反应性胶质细胞。超微结构变化更频繁,但被认为仅影响少数神经元。讨论了半暗带选择性电生理抑制的假说。

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