THE DISTRIBUTION OF HYPOGLYCEMIC BRAIN-DAMAGE
THE DISTRIBUTION OF HYPOGLYCEMIC BRAIN-DAMAGE
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DOI：
10.1007/bf00688108
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发表时间：
1984-01-01
影响因子：
12.7
通讯作者：
SIESJO, BK
中科院分区：
文献类型：
--
作者：
AUER, RN;WIELOCH, T;SIESJO, BK
大鼠暴露于胰岛素诱导的低血糖中，导致大脑等电时间范围为 10 至 60 分钟。用葡萄糖恢复后，他们被允许醒来并存活 1 周。对照大鼠在脑电图减慢阶段恢复。亚连续切片后，评估每个大脑区域中垂死神经元的数量和分布。人们发现酸性品红可以将垂死的神经元染成鲜红色。对照大鼠的大脑没有显示出死亡的神经元。从10分钟到60分钟的脑等电位，每个大脑死亡的神经元数量与脑等电位的分钟数呈正相关，直到最大检查时间60分钟。在容易受到几种不同损伤的主要大脑区域中发现了神经元坏死。在每个区域内，损伤的分布并不像缺血时所观察到的那样。在大脑皮层中观察到神经元坏死密度从浅到深的梯度。更严重的损伤也揭示了与下方白质相关的梯度。尾壳核在白质附近受累更严重，在侧脑室角附近受影响更严重的动物中。海马齿状回顶部出现密集的神经元坏死，CA1（前连合）内侧选择性神经元坏死呈梯度增加。 CA3区虽然相对有抵抗力，但在患有脑积水的动物中显示出与侧脑室相关的神经元坏死。在海马体中发现正常神经纤维和受损神经纤维之间存在明显的界限。室周杏仁核显示最靠近侧脑室的损伤。小脑在 Luschka 孔附近首先受到影响，受影响更严重的动物的半球也受到损害。浦肯野细胞首先受到影响，但篮子细胞也受到损害。脑干细胞核内可见罕见的坏死神经元。脊髓灰质所有区域的神经元均出现坏死。未见梗塞。组织液和脑脊液中携带的神经毒性物质可能导致低血糖脑损伤中神经元坏死的发病机制。
Rats were exposed to insulin-induced hypoglycemia resulting in periods of cerebral isoelectricity ranging from 10 to 60 min. After recovery with glucose they were allowed to wake up and survive for 1 wk. Control rats were recovered at the stage of EEG slowing. After sub-serial sectioning the number and distribution of dying neurons was assessed in each brain region. Acid fuchsin was found to stain moribund neurons a brilliant red. Brains from control rats showed no dying neurons. From 10 to 60 min of cerebral isoelectricity, the number of dying neurons per brain correlated positively with the number of minutes of cerebral isoelectricity up to the maximum examined period of 60 min. Neuronal necrosis was found in the major brain regions vulnerable to several different insults. Within each region the damage was not distributed as observed in ischemia. A superficial to deep gradient in the density of neuronal necrosis was seen in the cerebral cortex. More severe damage revealed a gradient in relation to the subjacent white matter as well. The caudatoputamen was involved more heavily near the white matter and in more severely affected animals near the angle of the lateral ventricle. The hippocampus showed dense neuronal necrosis at the crest of the dentate gyrus and a gradient of increasing selective neuronal necrosis medially in CA1 (commissura anterior). The CA3 zone, while relatively resistant, showed neuronal necrosis in relation to the lateral ventricle in animals with hydrocephalus. Sharp demarcations between normal and damaged neuropil were found in the hippocampus. The periventricular amygdaloid nuclei showed damage closest to the lateral ventricles. The cerebellum was affected 1st near the foramina of Luschka with damage occurring over the hemispheres in more severely affected animals. Purkinje cells were affected 1st but basket cells were damaged as well. Rare necrotic neurons were seen in brain stem nuclei. The spinal cord showed necrosis of neurons in all areas of the gray matter. Infarction was not seen. A neurotoxic substance borne in the tissue fluid and CSF may contribute to the pathogenesis of neuronal necrosis in hypoglycemic brain damage.