Kindgen-Milles D, Holthusen H
Heinrich-Heine-Universität Düsseldorf, Institut für Experimentelle Anaesthesiologie, Germany.
Eur J Pharmacol. 1997 Jun 5;328(1):41-4. doi: 10.1016/s0014-2999(97)83025-7.
To test the hypothesis that vascular pain depends on sympathetic drive under physiological conditions we studied the effects of both alpha-adrenoceptor stimulation by noradrenaline and alpha-adrenoceptor blockade by phentolamine on the intensity of physicochemically evoked pain from veins in humans. In seven healthy volunteers, a vascularly isolated hand vein segment was perfused continuously with noradrenaline (6 x 10(-9)-6 x 10(-6) M), or phentolamine (1.24 x 10(-4) M). Pain was evoked by intraluminal electrostimulation or by injection of hyperosmolar saline during control perfusion of isoosmolar saline and after each noradrenaline concentration, as well as after perfusion of phentolamine. Subjects rated pain intensity continuously on an electronically controlled visual analogue scale (VAS) between 0% VAS (no pain) and 100% VAS (tolerance maximum). Intravenous electrostimulation as well as hyperosmolar solutions evoked pain in each subject. The intensity of pain was neither influenced by noradrenaline, nor by phentolamine, so that nociception from blood vessels is unlikely to be modulated by the sympathetic nervous system under physiological conditions in humans.
为了验证在生理条件下血管性疼痛取决于交感神经驱动这一假说，我们研究了去甲肾上腺素对α-肾上腺素能受体的刺激作用以及酚妥拉明对α-肾上腺素能受体的阻断作用，二者对人体静脉内物理化学因素诱发疼痛强度的影响。在7名健康志愿者中，用去甲肾上腺素（6×10⁻⁹ - 6×10⁻⁶ M）或酚妥拉明（1.24×10⁻⁴ M）持续灌注一条血管隔离的手部静脉段。在等渗盐水对照灌注期间、每种去甲肾上腺素浓度之后以及酚妥拉明灌注后，通过腔内电刺激或注射高渗盐水诱发疼痛。受试者在电子控制的视觉模拟量表（VAS）上持续评定疼痛强度，范围为0% VAS（无疼痛）至100% VAS（最大耐受）。静脉电刺激以及高渗溶液在每个受试者中均诱发了疼痛。疼痛强度既不受去甲肾上腺素影响，也不受酚妥拉明影响，因此在人体生理条件下，血管的伤害感受不太可能受交感神经系统调节。
