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富含NADPH黄递酶阳性神经元的脊髓灰质层对缺血-再灌注诱导的损伤具有耐受性:一项对兔子的组织化学和银浸染研究

Spinal cord gray matter layers rich in NADPH diaphorase-positive neurons are refractory to ischemia-reperfusion-induced injury: a histochemical and silver impregnation study in rabbit.

作者信息

Marsala J, Kluchova D, Marsala M

机构信息

Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovak Republic.

出版信息

Exp Neurol. 1997 May;145(1):165-79. doi: 10.1006/exnr.1997.6455.

Abstract

Silver impregnation analysis of neuronal damage and concurrent histochemical characterization of NADPH diaphorase-positive neuronal pools in the rabbit lumbosacral segments was performed during and after transient spinal cord ischemia. Strongly enhanced staining of NADPH diaphorase-positive neurons and their processes appeared in the superficial dorsal horn (laminae I-III), the pericentral region (lamina X) of lower lumbar segments, the lateral collateral pathway, and mainly in neurons of the sacral parasympathetic nucleus in the S2 segment at the end of 40 min of abdominal aorta ligation or 1 day after reperfusion. Despite the development of extensive neuronal degeneration in the central gray matter (laminae IV-VII) between 1 and 4 days after ischemia, a number of nonnecrotizing neurons localized in the areas corresponding with the distribution of NADPH diaphorase-positive neurons was detected, suggesting a selective resistance of these classes of neurons against transient ischemic insult. While the precise mechanism of the observed resistance is not known, it is postulated that region-specific synthesis of nitric oxide and its vasodilatatory effect during the period of incomplete spinal ischemia may account for the observed selective resistance of these spinal cord neurons to transient ischemia.

摘要

在短暂性脊髓缺血期间及之后,对兔腰骶段神经元损伤进行银浸染分析,并对烟酰胺腺嘌呤二核苷酸磷酸黄递酶(NADPH diaphorase)阳性神经元池进行同步组织化学特征分析。在腹主动脉结扎40分钟末或再灌注1天后,在浅表背角(I-III层)、下腰段的中央周围区域(X层)、外侧副通路,以及主要在S2节段的骶副交感核神经元中,NADPH diaphorase阳性神经元及其突起的染色明显增强。尽管在缺血后1至4天中央灰质(IV-VII层)出现广泛的神经元变性,但在与NADPH diaphorase阳性神经元分布相对应的区域检测到一些非坏死性神经元,这表明这些类型的神经元对短暂性缺血损伤具有选择性抗性。虽然观察到的抗性的确切机制尚不清楚,但据推测,在不完全脊髓缺血期间一氧化氮的区域特异性合成及其血管舒张作用可能是这些脊髓神经元对短暂性缺血具有观察到的选择性抗性的原因。

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