Tanaka Satoshi, Barron Kirk W, Chandler Margaret J, Linderoth Bengt, Foreman Robert D
Department of Physiology, University of Oklahoma Health Sciences Center, PO Box 26901, Oklahoma City, OK 73190, USA.
Auton Neurosci. 2003 Mar 28;104(2):117-27. doi: 10.1016/S1566-0702(03)00017-1.
This study was performed to investigate the respective role of sensory afferent and sympathetic fibers in peripheral vasodilatation induced by spinal cord stimulation at different hindpaw skin temperatures. Cooling the skin was used as a strategy to enhance sympathetic activity [Am. J. Physiol.: Heart Circ. Physiol. 263 (1992) H1197]. Cutaneous blood flow in the footpad of anesthetized rats was recorded using laser Doppler flowmetry. Local cooling (<25 degrees C) or moderate local cooling (25-28 degrees C) of the hindpaw was produced with a cooling copper coil. Spinal cord stimulation delivered at clinically relevant parameters and with 30%, 60%, and 90% of motor threshold induced the early phase of vasodilatation in the cooled and the moderately cooled hindpaw. In addition, spinal cord stimulation at 90% of motor threshold produced the late phase of vasodilatation only in the cooled hindpaw, which was possible to block by the autonomic ganglion-blocking agent, hexamethonium. The early responses to spinal cord stimulation in the moderately cooled hindpaw were not affected by hexamethonium. In contrast, both the early and the late phase responses were eliminated by CGRP (8-37), an antagonist of the calcitonin gene-related peptide receptor. After dorsal rhizotomy, spinal cord stimulation at 90% of motor threshold elicited hexamethonium-sensitive vasodilatation in the cooled hindpaw (late phase). These results suggest that spinal cord stimulation-induced vasodilatation in the cooled hindpaw (<25 degrees C) is mediated via both the sensory afferent (early phase of vasodilatation) and via suppression of the sympathetic efferent activity (late phase) although the threshold for vasodilatation via the sympathetic efferent fibers is higher than that via sensory nerves. In contrast, vasodilatation via sensory afferent fibers may predominate with moderate temperatures (25-28 degrees C). Thus, two complementary mechanisms for spinal cord stimulation-induced vasodilatation may exist depending on the basal sympathetic tone.
本研究旨在探讨感觉传入纤维和交感神经纤维在不同后爪皮肤温度下脊髓刺激诱导的外周血管舒张中各自的作用。冷却皮肤被用作增强交感神经活动的一种策略[《美国生理学杂志：心脏循环生理学》263(1992)H1197]。使用激光多普勒血流仪记录麻醉大鼠足垫的皮肤血流量。用冷却铜线圈对后爪进行局部冷却(<25℃)或适度局部冷却(25 - 28℃)。以临床相关参数并分别为运动阈值的30%、60%和90%进行脊髓刺激，可在冷却和适度冷却的后爪中诱导血管舒张的早期阶段。此外，仅在冷却的后爪中，以运动阈值的90%进行脊髓刺激可产生血管舒张的晚期阶段，这一阶段可被自主神经节阻滞剂六甲铵阻断。六甲铵对适度冷却后爪中脊髓刺激的早期反应无影响。相比之下，降钙素基因相关肽受体拮抗剂CGRP(8 - 37)可消除早期和晚期反应。背根切断术后，以运动阈值的90%进行脊髓刺激在冷却的后爪中引发了六甲铵敏感的血管舒张(晚期阶段)。这些结果表明，脊髓刺激在冷却的后爪(<25℃)中诱导的血管舒张是通过感觉传入(血管舒张的早期阶段)和抑制交感传出活动(晚期阶段)介导的，尽管通过交感传出纤维实现血管舒张的阈值高于通过感觉神经的阈值。相比之下，在中等温度(25 - 28℃)下，通过感觉传入纤维的血管舒张可能占主导。因此，根据基础交感神经张力，可能存在两种互补的脊髓刺激诱导血管舒张的机制。
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