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神经外膜血管剥脱术后神经束膜下脱髓鞘与神经血流及氧分压降低相关。

Subperineurial demyelination associated with reduced nerve blood flow and oxygen tension after epineurial vascular stripping.

作者信息

Myers R R, Heckman H M, Galbraith J A, Powell H C

机构信息

Veterans Affairs Medical Center, San Diego, California.

出版信息

Lab Invest. 1991 Jul;65(1):41-50.

PMID:2072664
Abstract

Using laser Doppler measurements of nerve blood flow and electron microscopy, we determined that removal of the vasa nervorum from the surface of rat peripheral nerve results in an immediate 58.4% +/- (SD) 12.6% reduction in nerve blood flow (p less than 0.017) and subsequent subperineurial demyelination. To further assess the role of ischemia in demyelination, a second group of Sprague-Dawley rats (250 to 300 gm) was anesthetized and oxygen tensions were recorded with platinum microelectrodes in the tibial epineurial and endoneurial spaces before and 30 minutes after epineurial devascularization. Normal epineurial oxygen tension was 40.4 +/- (SD) 6.5 mm Hg before devascularization and 26.3 +/- 12.3 mm Hg after (p less than 0.012). Normal endoneurial oxygen tension was 22.9 +/- 6.0 mm Hg before devascularization and 14.3 +/- 5.4 mm Hg after (p less than 0.003). The topography of nerve fiber injury in this experimental model is identical with the changes induced in the sciatic nerve by circumferential compression at 30 mm Hg which is also thought to impede epineurial circulation. This subperineurial pattern of demyelination and axonal degeneration is associated with experimental interference with the epineurial circulation and may be contrasted with the central fascicular degeneration caused by microsphere embolization of the vasa nervorum via the common iliac artery. The data suggest that ischemia is the mechanism for subperineurial fiber injury after epineurial devascularization and highlight the importance of the transperineurial vessels which connect the epineurial anastomotic circulation and endoneurial capillary network.

摘要

通过激光多普勒测量神经血流并结合电子显微镜观察,我们发现从大鼠外周神经表面去除神经滋养血管会导致神经血流立即减少58.4%±(标准差)12.6%(p<0.017),随后出现神经束膜下脱髓鞘。为了进一步评估缺血在脱髓鞘中的作用,对第二组体重250至300克的Sprague-Dawley大鼠进行麻醉,并在神经束膜去血管化前和30分钟后,用铂微电极记录胫神经束膜和神经内膜间隙的氧张力。去血管化前正常的神经束膜氧张力为40.4±(标准差)6.5毫米汞柱,去血管化后为26.3±12.3毫米汞柱(p<0.012)。去血管化前正常的神经内膜氧张力为22.9±6.0毫米汞柱,去血管化后为14.3±5.4毫米汞柱(p<0.003)。该实验模型中神经纤维损伤的形态与坐骨神经在30毫米汞柱环周压迫下所诱导的变化相同,后者也被认为会阻碍神经束膜循环。这种神经束膜下脱髓鞘和轴突变性模式与对神经束膜循环的实验性干扰有关,并且可与通过髂总动脉对神经滋养血管进行微球栓塞所导致的中央束状变性形成对比。数据表明,缺血是神经束膜去血管化后神经束膜下纤维损伤的机制,并突出了连接神经束膜吻合循环和神经内膜毛细血管网络的跨神经束膜血管的重要性。

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Subperineurial demyelination associated with reduced nerve blood flow and oxygen tension after epineurial vascular stripping.神经外膜血管剥脱术后神经束膜下脱髓鞘与神经血流及氧分压降低相关。
Lab Invest. 1991 Jul;65(1):41-50.
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