PAIN, HYPERALGESIA AND ACTIVITY IN NOCICEPTIVE-C UNITS IN HUMANS AFTER INTRADERMAL INJECTION OF CAPSAICIN

PAIN, HYPERALGESIA AND ACTIVITY IN NOCICEPTIVE-C UNITS IN HUMANS AFTER INTRADERMAL INJECTION OF CAPSAICIN
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DOI:
10.1113/jphysiol.1992.sp019068
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发表时间:
1992-03-01
影响因子:
5.5
通讯作者:
TOREBJORK, HE
TOREBJORK, HE
中科院分区:
医学1区
文献类型:
--
作者:
LAMOTTE, RH;LUNDBERG, LER;TOREBJORK, HE

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1. 辣椒素是辣椒中有效的止痛物质,在清醒的人类中局部应用,或皮下注射到14c机械热(多模态)伤害感受器单元的接受野内或外。用插入腓神经的微电极记录痛觉感受器放电。同时,受试者在注射后1.5-3分钟内估计疼痛程度作为时间的函数。为了评估皮肤痛觉过敏的程度,在使用辣椒素之前和之后,还获得了由热和/或机械刺激产生的疼痛程度的估计值。在C伤害感受器单元的感受野内或附近注射,但不大于4毫米外,可引起放电。疼痛强度和平均放电率均在注射时达到最大,并在随后的1-3 min内迅速下降,这表明这些伤害感受器与辣椒素注射引起的疼痛强度和持续时间有关。辣椒素注射后感受野C痛觉感受器兴奋性降低或消失与注射部位的镇痛相关。辣椒素注射产生大面积的机械性痛觉过敏,即轻触皮肤时疼痛或点状刺激时异常剧烈的疼痛。然而,注射并没有降低阈值,也没有增强C伤害感受器单位对这种机械刺激的反应,它们在这个痛觉过敏区域的感受野。局部应用辣椒素诱发持续放电在四个单位测试。当温度从45摄氏度降至35摄氏度时,伤害感受器反应阈值和疼痛阈值都降低了。5 .在服用辣椒素后,以两单位轻触皮肤后出现的一种新出现的微弱反应,并伴有轻微疼痛。敏化C伤害感受器的持续活动和伴随的疼痛通过冷却接受区域的皮肤有效地减少。由此得出结论,C机械热(多模态)伤害感受器的活性与皮内注射辣椒素引起的疼痛的强度和持续时间有关。辣椒素对C伤害感受器兴奋性的后效取决于浓度:高浓度(注射)导致脱敏,而低浓度(外用)导致致敏。在局部应用辣椒素后,这些单位的持续放电和对热的反应阈值降低与背景疼痛以及受影响皮肤对热的疼痛阈值降低相关(原发性痛觉过敏)。注射区外皮肤C痛觉感受器的反应性不变,表明中枢而非外周致敏导致了该区域观察到的机械性痛觉过敏(继发性痛觉过敏)。
1. Capsaicin, the potent algesic substance in chilli peppers, was applied topically to, or injected intradermally into or outside, the receptive fields of 14 C mechanoheat (polymodal) nociceptor units in awake humans. The nociceptor discharges were recorded using microelectrodes inserted into the peroneal nerve. Simultaneously, the subjects estimated the magnitude of pain as a function of time during the first 1.5-3 min after injection. Magnitude estimates of pain produced by heat and/or mechanical stimuli were also obtained before and after capsaicin in order to assess the magnitude of cutaneous hyperalgesia.2. An injection within or adjacent to, but not greater than 4 mm outside, the receptive fields of C nociceptor units evoked discharges. The magnitude of pain and the mean discharge rate of the units were both maximal on injection, declining rapidly over the next 1-3 min, which indicates that these nociceptors contribute to the magnitude and duration of pain evoked by capsaicin injection.3. Reduced or abolished excitability in C nociceptors after capsaicin injection within the receptive fields correlated with analgesia at the injection site.4. Capsaicin injection produced a wide surround area of mechanical hyperalgesia, i.e. pain on gently stroking the skin or abnormally intense pain on punctate stimulation. Nevertheless, the injections did not lower the thresholds or enhance the responses to such mechanical stimuli of C nociceptor units with their receptive fields in this hyperalgesic area.5. Topical application of capsaicin evoked on-going discharges in four units tested. Both nociceptor response thresholds and pain thresholds were lowered for heat from 45 to 35-degrees-C. A newly developed weak response to stroking the skin in two units after capsaicin was accompanied by faint pain.6. On-going activity in sensitized C nociceptors and concomitant pain were effectively reduced by cooling the skin in the receptive area.7. It is concluded that activity in C mechanoheat (polymodal) nociceptors contributes to the magnitude and duration of pain evoked by intradermal injection of capsaicin. The after-effects of capsaicin on C nociceptor excitability depend on concentration: high concentration (by injection) leads to desensitization, whereas low concentration (by topical application) leads to sensitization. On-going discharges and lowered response thresholds to heat in these units after topical application of capsaicin correlates with background pain as well as lowered pain thresholds to heat of the affected skin (primary hyperalgesia). The unchanged responsiveness of C nociceptors in the skin well outside the injection area indicates that central rather than peripheral sensitization accounts for the observed mechanical hyperalgesia in this region (secondary hyperalgesia).