MITOCHONDRIAL LESION IN EXPERIMENTAL SPINAL-CORD TRAUMA
MITOCHONDRIAL LESION IN EXPERIMENTAL SPINAL-CORD TRAUMA
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DOI：
10.3171/jns.1978.48.3.0434
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发表时间：
1978-01-01
影响因子：
4.1
通讯作者：
YASHON, D
中科院分区：
文献类型：
--
作者：
ITO, T;ALLEN, N;YASHON, D
用显微分光光度法测定了犬脊髓灰质和白质的显微解剖标本的细胞色素氧化酶活性。实验动物在T-3至T-4水平受到400g-cm的冲击力。在损伤部位中央、距损伤中心1 mm处和非损伤节段取材进行酶分析和组织学研究。细胞色素氧化酶活性早在创伤后15min就下降到正常值的50%左右，创伤中心下降幅度最大，距离越远影响越小。这种效应与已知的线粒体脊和内膜的形态缺陷有关。酶的变化与灰质和神经元损伤的组织学评估显著相关，但也部分独立于这些过程。创伤部位白质中酶活性的小幅但显著增加被认为最有可能是由于轴浆流动受损而导致的线粒体积聚。
Cytochrome oxidase activities were determined by a microspectrophotometric method on microdissected samples of gray and white matter from frozen-dried sections of dog spinal cord. Experimental animals received 400 g-cm impact at the T-3 to T-4 level. Sections for enzyme analysis and histological study were taken at the center of the trauma site, at successive 1 mm distances from the center and at non-traumatized segments. A drop in cytochrome oxidase activities to approximately 50% of normal value was found as early as 15 min post-trauma, with greatest decrease at the trauma center and lesser effects at successive distances. This effect was related to known morphological defects in mitochondrial cristae and inner membranes. The enzyme change was significantly correlated with histological estimates of gray matter and neuronal damage, but was also partially independent of these processes. A small but significant increase of enzyme activity in white matter at the trauma site was considered most likely attributable to mitochondrial accumulations due to impaired axoplasmic flow.