Division of Neurology, University of Calgary, Calgary, Alberta, Canada.
J Neurotrauma. 2010 Mar;27(3):639-46. doi: 10.1089/neu.2009.1025.
The microvascular supply of the peripheral nerve trunk may be rendered vulnerable by acute focal injuries, particularly if they are associated with direct injury to the epineurial blood supply. In this work we tracked the impact of three clinically relevant forms of focal nerve trunk injury on serial measures of epineurial weighted erythrocyte flux and endoneurial blood flow: short-length crush injuries, long-segmental crush injuries, and crush injuries with superimposed vascular stripping to model added direct epineurial damage. Red blood cell (RBC) flux was measured using quantitative multiple sampling laser doppler flowmetry, and endoneurial blood flow by microelectrode hydrogen clearance polarography. Both short and long crush injuries transiently reduced epineurial RBC flux, most prominently in long injuries, to 34% by 1 h after injury. The changes were less prominent when deeper flux was examined, whereas endoneurial blood flow was not altered by either injury. Long crush injury with added stripping of the epineurial blood supply was associated with more profound declines in epineurial RBC flux, to 16% by 3 h, with recovery at 14 days to 70% of that of the contralateral intact nerve trunk. There was, however, only a minimal impact on endoneurial flow: mild reductions immediately and at 1 h after injury, with rebound hyperemia by 48 h. Despite the presence of prominent epineurial ischemia, regenerative sprouting was not impaired by longer segmental injuries with or without epineurial vascular stripping. Axon sprouting was more prominent in both of these types of injuries compared to short-crush lesions. Taken together, these results indicate that focal nerve trunk injury is remarkably resistant to endoneurial ischemia, and that it can sustain regenerative sprouting in spite of prolonged alterations in the epineurial circulation. Approaches to augment epineurial microvascular viability after nerve injury may not support better regeneration.
周围神经干的微血管供应可能因急性局灶性损伤而变得脆弱，尤其是当这些损伤与神经外膜血供的直接损伤有关时。在这项工作中，我们跟踪了三种临床相关的局灶性神经干损伤对神经外膜加权红细胞通量和神经内膜血流的连续测量的影响：短长度挤压伤、长节段挤压伤和挤压伤伴有外加的血管剥离以模拟外加的直接神经外膜损伤。使用定量多点激光多普勒流量测定法测量红细胞（RBC）通量，使用微电极氢清除极谱法测量神经内膜血流。短挤压伤和长挤压伤都短暂地降低了神经外膜 RBC 通量，在受伤后 1 小时最明显，降低到 34%。当检查更深的血流量时，变化不那么明显，而神经内膜血流不受任何一种损伤的影响。伴有外加的神经外膜血供剥离的长挤压伤与神经外膜 RBC 通量的更显著下降有关，在 3 小时时下降到 16%，在 14 天时恢复到对侧完整神经干的 70%。然而，对神经内膜血流只有轻微影响：受伤后即刻和 1 小时轻度减少，48 小时时出现反弹性充血。尽管存在明显的神经外膜缺血，但较长节段的损伤，无论是否有神经外膜血管剥离，都不会损害再生发芽。与短挤压损伤相比，这两种类型的损伤中轴突发芽更为明显。总之，这些结果表明，局灶性神经干损伤对神经内膜缺血具有很强的抵抗力，并且尽管神经外膜循环发生了长时间的改变，它仍能维持再生发芽。在神经损伤后增加神经外膜微血管活力的方法可能并不能支持更好的再生。
