Effect of naloxone on primary and secondary hyperalgesia induced by the human burn injury model

Effect of naloxone on primary and secondary hyperalgesia induced by the human burn injury model
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DOI:
10.1034/j.1399-6576.2001.450806.x
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发表时间:
2001-09-01
影响因子:
2.1
通讯作者:
Dahl, JB
Dahl, JB
中科院分区:
医学4区
文献类型:
--
作者:
Brennum, J;Kaiser, F;Dahl, JB

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背景:阿片拮抗剂可能改变实验性痛觉过敏模型的反应。这表明内源性阿片系统可能参与了这些模型。本研究的目的是通过静脉注射非选择性阿片拮抗剂纳洛酮,评估内源性阿片系统的激活是否可以在皮肤痛觉过敏的人体烧伤模型中得到证明。方法:我们采用随机、双盲、三重交叉设计研究了25名年龄在20-31岁的健康男性志愿者。在犊牛上形成25 X 50 mm矩形烧伤,间隔至少1周,时间为3天。受试者在烧伤诱导后3小时静脉注射纳洛酮0.4 mg、10 mg或安慰剂。结果:烧伤可引起原发性和继发性痛觉过敏。纳洛酮不影响任何测量变量:非损伤或损伤组织的热痛检测阈值,非损伤或损伤组织的短时间或长时间有害热引起的疼痛,针刺或中风引起的继发性痛觉过敏,或短时间或长时间的有害机械刺激引起的非损伤组织的疼痛。纳洛酮未出现明显不良反应。结论:内源性阿片类药物反应在人类志愿者烧伤引起痛觉过敏后的激活不能通过静脉注射纳洛酮来证明。这些发现表明,内源性阿片反应不是该模型的混杂因素。
Background: Opioid antagonists may change the responses in models of experimental hyperalgesia. This indicates a possible involvement of the endogenous opioid system in these models. The aim of the present study was to evaluate whether activation of the endogenous opioid system could be demonstrated in the human burn injury model of cutaneous hyperalgesia, using an intravenous challenge with the non-selective opioid antagonist naloxone.Methods: We studied 25 healthy male volunteers aged 20-31 yrs in a randomised, double-blind, triple crossover design. A 25 X 50 mm rectangular burn injury was produced on the calf on 3 separate days, at least I week apart. Subjects received an intravenous bolus dose of naloxone 0.4 mg, 10 mg or placebo 3 h after induction of the burn injury.Results: Primary and secondary hyperalgesia was induced by the burn injury. Naloxone did not affect any of the measured variables: heat pain detection threshold in non-injured or injured tissue, pain produced by short or prolonged noxious heat in non-injured or injured tissue, secondary hyperalgesia elicited by pin prick or stroke, or pain produced by short or prolonged noxious mechanical stimulation in non-injured tissue. No significant adverse effects of naloxone were encountered.Conclusions: Activation of an endogenous opioid response following induction of hyperalgesia in human volunteers by a burn injury could not be demonstrated with an intravenous naloxone challenge. These findings suggest that the endogenous opioid response is not a confounding factor in this model.