Hoffmann P, Carlsson S, Thorén P
Department of Physiology, University of Gothenburg, Sweden.
Acta Physiol Scand. 1990 Nov;140(3):353-8. doi: 10.1111/j.1748-1716.1990.tb09009.x.
In a previous study, prolonged low-frequency muscle stimulation, inducing dynamic contractions in the hind leg of unanaesthetized rats, was shown to give rise to a hypoalgesia. The increase in pain threshold, measured as squeak threshold to noxious electric pulses, lasted 3 h. In the present study, the involvement of the endogenous opioid system in the post-stimulatory analgesia was investigated using selective opioid receptor antagonists. The post-stimulatory analgesia was completely reversed back to prestimulatory control levels by naloxone, 1 mg kg-1. ICI 154,129 and MR 2266 BS, selective delta- and kappa-receptor antagonists respectively, did not significantly influence the post-stimulatory analgesia, although ICI 154,129 had a minor pain threshold-lowering effect. Rats pretreated with beta-funaltrexamine, a mu-receptor antagonist, did not exhibit any post-stimulatory analgesia. These results suggest that opioid systems are involved in the increase in pain threshold after muscle stimulation and that the analgesic response is both elicited and maintained by the mu-receptor.
在先前的一项研究中，对未麻醉大鼠的后腿进行长时间低频肌肉刺激以诱发动态收缩，结果显示会产生痛觉减退。以对有害电脉冲的 squeak 阈值衡量的疼痛阈值升高持续了 3 小时。在本研究中，使用选择性阿片受体拮抗剂研究了内源性阿片系统在刺激后镇痛中的作用。1 mg kg-1 的纳洛酮可使刺激后镇痛完全恢复到刺激前的对照水平。ICI 154,129 和 MR 2266 BS 分别为选择性 δ 和 κ 受体拮抗剂，尽管 ICI 154,129 有轻微降低疼痛阈值的作用，但并未显著影响刺激后镇痛。用 μ 受体拮抗剂 β-氟纳曲明预处理的大鼠未表现出任何刺激后镇痛。这些结果表明，阿片系统参与了肌肉刺激后疼痛阈值的升高，并且镇痛反应由 μ 受体引发并维持。
