Zochodne D W, Ho L T
Peripheral Nerve Research Laboratory, Queen's University, Kingston, Ont., Canada.
Brain Res. 1992 Dec 11;598(1-2):59-66. doi: 10.1016/0006-8993(92)90168-9.
Intrinsic mechanisms of vasodilatation may prevent injury-related ischemia in peripheral nerve endoneurium. We examined local perfusion up to 10 days following local crush, partial injury or simple exposure of the rat sciatic nerve. By employing epineurial hCGRP(8-37), a receptor antagonist of CGRP, and serial hydrogen clearance measurements, we estimated the component of post-injury blood flow related to local CGRP action. Injury-related ischemia was not observed at any of the time points studied at or proximal to injury. Instead, endoneurial blood flow (EBF) increased at 24 h proximal to crush or partial injury, and at 48 h within the crush zone when compared to sham operated controls or to a pooled reference range of EBF. Composite blood flow (F) was also elevated at 48 h and 5 days within the crush zone suggesting hyperemia involving the epineurial plexus, perineurial vessels and AV shunts. hCGRP(8-37) constricted vasa nervorum at most time points but its effect on EBF was maximum and exceeded controls within the crush zone at 48 h. The findings indicate that certain types of nerve injury, including focal crush, are associated with hyperemia, not ischemia. CGRP vasodilatation may account for part of this response, implying a local peptidergic afferent fiber response to nerve trunk injury.
血管舒张的内在机制可能预防外周神经内膜中与损伤相关的缺血。我们检测了大鼠坐骨神经局部挤压、部分损伤或单纯暴露后长达10天的局部灌注情况。通过使用降钙素基因相关肽（CGRP）的受体拮抗剂——神经外膜hCGRP(8 - 37)，以及连续的氢清除率测量，我们估算了与局部CGRP作用相关的损伤后血流成分。在损伤处或损伤近端所研究的任何时间点均未观察到与损伤相关的缺血。相反，与假手术对照组或EBF的汇总参考范围相比，在挤压或部分损伤近端24小时时神经内膜血流（EBF）增加，在挤压区域内48小时时EBF也增加。在挤压区域内48小时和5天时，复合血流（F）也升高，提示充血累及神经外膜丛、神经束膜血管和动静脉分流。hCGRP(8 - 37)在大多数时间点使神经血管收缩，但其对EBF的影响在48小时时在挤压区域内最大且超过对照组。这些发现表明，某些类型的神经损伤，包括局灶性挤压，与充血而非缺血相关。CGRP介导的血管舒张可能是这种反应的部分原因，这意味着存在对神经干损伤的局部肽能传入纤维反应。
