NERVE BLOOD FLOW IN NORMAL AND ISCHEMIC PERIPHERAL NERVE

周围神经依赖神经血流量（NBF）提供能量 要求. 由于哺乳动物的外周神经不自动调节，NBF 严重依赖于毛细血管间距、结构、交感神经 神经支配，以及神经因素如BP和粘度。 在 水肿性神经病，如Dejerine Sottas神经病、肥大性 腓骨肌萎缩症和 泼尼松反应性遗传性运动和感觉神经病 继发于毛细血管间增加的神经内膜缺氧的可能性 距离 交感神经支配、毛细血管结构和 血液粘稠度也发生在人类周围神经病中。 是 因此，重要的是检查正常和异常NBF的生理学， 神经 待检验的广泛假设是缺血性神经病 当神经血流的幅度和持续时间减少超过 缺血安全系数。 我们假设神经缺血安全因子 可以根据压力、神经血流反应和 代谢效应，如果这些被量化。 因此，我们建议对神经血流进行以下研究。 1)交感神经刺激和切断对神经血流量的影响。 2)神经刺激对神经血流量的影响。 3)的影响 降低血压对神经血流量和能量代谢的影响。 4)的 微栓子对神经血流量和能量代谢影响 5)到 确定局部缺血对中枢是否有不同的影响， 在3和4中列出的扰动下的束的外围。 我们 将检查NBF中是否存在径向地形分布， 神经水肿 在进行最后两项研究时，将记录NBF 同时使用插入到纤维束中心的微量移液管 进入神经束膜下区域 6)均与 以上记录的神经乳酸盐测量值（缺氧指数） 代谢）和核苷酸磷酸（腺苷三磷酸和肌酸 磷酸盐），以提供对缺血影响的估计 关于能量代谢

Peripheral nerve depends on nerve blood flow (NBF) for its energy requirements. Since mammalian peripheral nerve does not autoregulate, NBF is critically dependent on intercapillary distance, structure, sympathetic innervation, and on extraneural factors such as BP, and viscosity. In the edematous neuropathies such as Dejerine Sottas neuropathy, hypertrophic Charcot-Marie-Tooth disease and prednisone-responsive-hereditary-motor-and-sensory-neuropathy there is the potential of endoneurial hypoxia secondary to increased intercapillary distance. Alterations in sympathetic innervation, capillary structure and blood viscosity also occur in human peripheral neuropathies. It is therefore important to examine the physiology of NBF in normal and abnormal nerves. The broad hypothesis to be tested is that ischemic neuropathy develops when nerve blood flow is reduced in magnitude and duration beyond its ischemia safety factor. We postulate that nerve ischemia safety factor may be definable in terms of the stress, the nerve blood flow response and the metabolic effects if these were quantitated. We therefore propose to do the following studies on nerve blood flow. 1) The effect of sympathetic stimulation and section on nerve blood flow. 2) The effect of nerve stimulation on nerve blood flow. 3) The effects of blood pressure reduction on nerve blood flow and energy metabolism. 4) The effect of microemboli on nerve blood flow and energy metabolism. 5) To determine if there is a differential effect of ischemia on the center and the periphery of the fascicle under perturbations listed in 3 and 4. We will examine if there is a radial topographic distribution in NBF in edematous nerves. To do the last two studies, NBF will be recorded simultaneously using micropipets inserted into the center of the fascicle and into the subperineurial region of the fascicle. 6) Pari passu with the above recordings measurements of nerve lactate (an index of anerobic metabolism) and nucleotide phosphates (adenosine triphosphate and creatine phosphate) will be made to provide an estimate of the effects of ischemia on energy metabolism.