NERVE DESTRUCTION BY COLCHICINE IN MICE AND GOLDEN HAMSTERS
NERVE DESTRUCTION BY COLCHICINE IN MICE AND GOLDEN HAMSTERS
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DOI：
10.1002/jez.1401360209
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发表时间：
1957-01-01
影响因子：
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通讯作者：
ANGEVINE, JB
中科院分区：
文献类型：
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作者：
ANGEVINE, JB
当秋水仙碱直接注入哺乳动物神经时，只要浓度超过0.01，就会引起广泛的退变[图像]组织学研究显示，在输液部位远端有明显的向心性退变，逆行损伤长达15毫米。然而，由于哺乳动物大体积的稀释效应，神经系统的其他部分不会发生退化。退变的开始时间通常比沃勒退变观察到的时间要晚。Meso-inositol仅轻微抑制秋水仙碱的作用，而ATP则在速度和严重程度上大大增加秋水仙碱的作用。在仓鼠脑内注射秋水仙碱，显示出对中毒的抵抗力不比小鼠强，而注射坐骨神经则产生了上述组织病理学。根据这些发现，考虑到仓鼠对秋水仙碱的已知抗药性。
Colchicine when infused directly into mammalian nerve causes extensive degeneration provided the concentration exceeds 0.01 [image] Histological studies revealed an apparently centripetal degeneration distal to the infusion site and retrograde damage extending as far as 15 mm. Degeneration in other parts of the nervous system does not occur, however, due to the diluting effect of the large body volume of the mammal. Initiation of degeneration was usually delayed beyond the time observed for Wallerian degeneration. Meso-inositol inhibited only slightly the colchicine effect, whereas ATP greatly increased it in speed and severity. Intracerebral administration of colchicine in the hamster revealed resistance to intoxication no greater than in the mouse and infusion of the sciatic produced the histopathology noted above. The known resistance of the hamster to colchicine is considered in light of these findings.