Wakisaka Satoshi, Kajander Keith C, Bennett Gary J
Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892 U.S.A.
Pain. 1991 Sep;46(3):299-313. doi: 10.1016/0304-3959(91)90113-C.
A chronic constriction injury to the sciatic nerve of the rat produces a neuropathic pain syndrome that has many of the symptoms that are seen in humans with painful peripheral neuropathy. In particular, both the clinical and experimental conditions are accompanied by an abnormality of cutaneous temperature regulation in the painful area. A time course study was made of this phenomenon in the experimental model. In normal rats, there is little or no difference between the temperature of the two hind paws (plantar skin). After nerve injury, however, approximately 75% of the rats (N = 30) had abnormally large (greater than +/- 0.9 degrees C) temperature differences (delta T) between the affected and sham-operated sides. The abnormal delta Ts could be either positive or negative, i.e., the affected side could be hotter or colder than normal. For individual cases, the temperature abnormality was highly variable over time periods of hours to days; abnormally hot skin could switch to being abnormally cold, and vice versa, and small delta Ts in the normal range could switch between abnormal extremes. Despite this individual variability, the average delta T of the group as a whole displayed a clear evolution over the course of the 30-day observation period: abnormally hot initially and progressing to abnormally cold. A parallel time course study was made of the status of the sympathetic vasoconstrictor innervation to the affected hind paw (plantar artery and vein). As demonstrated with a histofluorescence method that visualizes catecholamines, there was a gradual loss of norepinephrine (NE)-containing sympathetic efferents on the nerve-injured side. The decrease was first noted on postoperative day 5 (PO5), was very marked by PO10-PO14, and progressed to a complete or nearly complete loss by PO30. There was a concomitant decrease in staining for two other substances found in vasoconstrictor efferents, dopamine-beta-hydroxylase (DBH) and neuropeptide Y (NPY). The NE-containing innervation of the contralateral (sham-operated) plantar vessels appeared to be normal at all times. Lastly, in order to determine whether there was any relation between the temperature abnormality and the status of the sympathetic perivascular plexus, additional rats were sacrificed immediately after skin temperature measurement and the hind paw vessels were stained for NE. The vasculature of some abnormally cold paws had no detectable NE. Some rats that did not appear to have a temperature abnormality also had no detectable NE on the affected hind paw's vasculature. The vasculature of some abnormally hot paws had normal NE.(ABSTRACT TRUNCATED AT 400 WORDS)
对大鼠坐骨神经进行慢性压迫损伤会引发一种神经性疼痛综合征，该综合征具有许多人类疼痛性周围神经病变所呈现的症状。特别是，临床和实验条件下，疼痛区域的皮肤温度调节均出现异常。在该实验模型中对这一现象进行了时间进程研究。正常大鼠的两只后爪（足底皮肤）温度几乎没有差异或完全相同。然而，神经损伤后，约75%的大鼠（N = 30）在患侧与假手术侧之间出现异常大的（大于+/- 0.9摄氏度）温差（ΔT）。异常的ΔT可为正值或负值，即患侧可能比正常更热或更冷。对于个体情况，数小时至数天内温度异常变化很大；异常热的皮肤可能转变为异常冷，反之亦然，正常范围内的小ΔT可能在异常极值之间切换。尽管存在个体差异，但在30天的观察期内，整个组的平均ΔT呈现出明显的变化过程：最初异常热，随后发展为异常冷。对患侧后爪（足底动脉和静脉）的交感缩血管神经支配状态进行了平行的时间进程研究。通过一种可视化儿茶酚胺的组织荧光方法显示，神经损伤侧含去甲肾上腺素（NE）的交感传出神经逐渐减少。术后第5天（PO5）首次发现减少，PO10 - PO14时非常明显，到PO30时发展为完全或几乎完全丧失。在缩血管传出神经中发现的另外两种物质，多巴胺-β-羟化酶（DBH）和神经肽Y（NPY）的染色也随之减少。对侧（假手术）足底血管的含NE神经支配在所有时间似乎都正常。最后，为了确定温度异常与交感血管周围丛的状态之间是否存在任何关联，在测量皮肤温度后立即处死另外一些大鼠，并对后爪血管进行NE染色。一些异常冷的爪子的血管系统未检测到NE。一些似乎没有温度异常的大鼠，其患侧后爪血管系统也未检测到NE。一些异常热的爪子的血管系统NE正常。（摘要截选至400字）
