Lim R K, Krauthamer G, Guzman F, Fulp R R
Proc Natl Acad Sci U S A. 1969 Jul;63(3):705-12. doi: 10.1073/pnas.63.3.705.
Synthetic bradykinin, a nonapeptide formed from alpha-2 globulin in plasma, injected intra-arterially or intraperitoneally in cats in doses of 10-50 mug, evoked activity in the central nervous system in pathways associated with the signaling of pain. Similar injections of bradykinin in intact normal cats and dogs evoked manifestations of pain, and in conscious humans elicited verbal reports of pain perceived in the area of injection. Single unit activity was recorded in the medial reticular formation of the brainstem, in the medial thalamus and, more laterally, among the posterior group nuclei and the suprageniculate nucleus. Bradykinin did not evoke any cortical or subcortical slow potentials such as those evoked by electrical stimulation of the foot pads. When bradykinin was given together with the electrical stimulus, the responses evoked by the latter were blocked. Morphines uppressed bradykinin-evoked activity. Aspirin caused marked fluctuations in activity, unrelated to the bradykinin injection; the bradykinin block of evoked potentials could no longer be observed after aspirin dosage. The results are discussed in terms of the peripheral and central sites of analgesic action and the likelihood of the existence of chemosensitive pain receptors.
合成缓激肽是一种由血浆中的α-2球蛋白形成的九肽，以10 - 50微克的剂量动脉内或腹腔内注射到猫体内时，会在与疼痛信号传导相关的中枢神经系统通路中引发活动。在完整的正常猫和狗身上进行类似的缓激肽注射会引发疼痛表现，在清醒的人类中会引发关于注射部位疼痛的口头报告。在脑干的内侧网状结构、内侧丘脑以及更外侧的后组核和上膝状体核中记录到了单个单位活动。缓激肽不会引发任何皮质或皮质下慢电位，如电刺激脚垫所引发的慢电位。当缓激肽与电刺激一起给予时，后者所引发的反应会被阻断。吗啡抑制缓激肽引发的活动。阿司匹林导致活动出现明显波动，这与缓激肽注射无关；在给予阿司匹林剂量后，不再能观察到缓激肽对诱发电位的阻断作用。从镇痛作用的外周和中枢部位以及化学敏感疼痛感受器存在的可能性方面对结果进行了讨论。
