Price Donald D, Hu James W, Dubner Ronald, Gracely Richard H
Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Md. 20014, U.S.A.
Pain. 1977 Feb;3(1):57-68. doi: 10.1016/0304-3959(77)90035-5.
Psychophysical experiments were carried out on 6 huma subjects to determine how first and second pain are influenced by peripheral receptor mechanisms and by central nervous system inhibitory and facilitatory mechanisms. For these experiments, brief natural painful stimuli delivered to the hand were a train of 4-8 constant waveform heat pulses generated by a contact thermode (peak temp. = 51-5% C). The magnitude of first and second pain sensations was estimated using cross-modality matching procedures and reaction times were determined. The latter confirmed the relationship between first and second pain and impulse conduction in Adelta and C noxious heat afferents, respectively. The intensity of first pain decreased with each successive heat pulse when the interpulse interval was 80 sec or less. This decrease was most likely the result of heat induced suppression of Adelta heat nociceptors since it did not occur if the probe location changed between successive heat pulses. In contrast, second pain increased in intensity with each successive heat pulse if the interval was 3 sec or less. This summation was most likely due to central nervous system summation mechanisms since it also occurred after blockage of first pain by ulnar nerve compression and when the location of the thermode changed between heat pulses. These observations and their interpretations are supported by our recording of responses of singlt Adelta heat nociceptive afferents, C polymodal nociceptive afferents, and "warm" afferents of rhsus monkeys to similar trains of noxious heat pulses. Their responses to these heat pulses show a progressive suppression. Furthermore, previous studies have shown that wide dynamic range dorsal horn neurons show summated responses to repeated volleys in C fibers (greater than 1/3 sec). These spinal cord summation mechanisms could account for the summation of second pain.
对6名人类受试者进行了心理物理学实验，以确定第一痛和第二痛如何受到外周感受器机制以及中枢神经系统抑制和易化机制的影响。在这些实验中，施加于手部的短暂自然疼痛刺激是由接触式热刺激器产生的一串4 - 8个恒定波形的热脉冲（峰值温度 = 51 - 55℃）。使用交叉模式匹配程序估计第一痛和第二痛觉的强度，并测定反应时间。后者分别证实了第一痛和第二痛与Aδ和C伤害性热传入纤维中冲动传导之间的关系。当脉冲间隔为80秒或更短时，随着连续热脉冲的增加，第一痛的强度降低。这种降低很可能是热诱导的Aδ热伤害感受器抑制的结果，因为如果在连续热脉冲之间探头位置发生变化，这种情况就不会发生。相比之下，如果间隔为3秒或更短时，第二痛的强度会随着连续热脉冲而增加。这种总和很可能是由于中枢神经系统的总和机制，因为在尺神经压迫阻断第一痛后以及热刺激器在热脉冲之间位置改变时也会发生这种情况。我们对恒河猴的单个Aδ热伤害性传入纤维、C多模式伤害性传入纤维和“温觉”传入纤维对类似的有害热脉冲序列的反应记录支持了这些观察结果及其解释。它们对这些热脉冲的反应显示出逐渐抑制。此外，先前的研究表明，广动力范围的背角神经元对C纤维中的重复群集（大于1/3秒）表现出总和反应。这些脊髓总和机制可以解释第二痛的总和现象。
