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The beta-adrenergic receptor agonist, terbutaline, reduces UVB-induced mechanical sensitization in humans

机译:β-肾上腺素能受体激动剂特布丁醛可降低人类的UVB诱导的机械敏化

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摘要

Objectives Previously, we found in cultures of primary neurons and in animals that sensitized primary neurons can be desensitized by treatment with e.g. beta-adrenergic receptor agonists. We now tested whether also in human sensitization such as UVB-radiation induced sunburn-like hyperalgesia can be reduced by intradermal injection of the beta-adrenergic receptor agonist terbutaline. Methods In our prospective randomized study, 17 participants received an individual UVB dose to cause a defined local sunburn-like erythema at four locations, two on each forearm. Twenty-four hours later, the sensitized four areas were injected intradermally with terbutaline pH 4.3, terbutaline pH 7.0, saline pH 4.3 or saline pH 7.0, respectively. Pain thresholds were examined before and after induction of UVB-sensitization, and 15, 30 and 60 min after injection of the respective solution. Mechanical pain thresholds of the skin and of deeper tissues were determined by pinprick and pressure algometer measurements, respectively. Results UVB-irradiation decreased mechanical pain thresholds for pinprick and pressure algometer measurements demonstrating a successful sunburn-like sensitization. Intradermal injection of terbutaline pH 7.0 into the sensitized skin reduced the sensitization for all measured timepoints as determined by pinprick measurements. Pinprick measurements of sensitization were not reduced by injection of terbutaline pH 4.3, saline solution pH 7.0 or saline solution pH 4.3. Also, sensitization of deeper tissue nociceptors were not altered by any of the injections as measured with the pressure algometer. Conclusions Similar to our cellular observations, also in humans beta-adrenergic agonists such as terbutaline can reduce the sensitization of primary neurons in the skin. Significance We previously showed in model systems that beta-adrenergic stimulation can not only sensitize but also desensitize nociceptors. Our study shows that also in humans beta-adrenergic agonists desensitize if injected into UVB-sensitized skin. This indicates an analgesic activity of adrenergic agonists in addition to their vasoconstrictory function.
机译:以前,我们发现在原发性神经元和敏感的原发性神经元的培养物中发现可以通过用例如敏化的原代神经元进行培养。 β-肾上腺素能受体激动剂。我们现在测试了人类致敏等诸如UVB-辐射诱导的晒斑样痛觉体,可以通过皮内注射β-肾上腺素能受体激动剂特布布丁来降低。方法在我们的前瞻性随机研究中,17名参与者接受了个体UVB剂量,以在每个前臂上导致四个地点的局部晒伤的红斑,两种位置。二十四小时后,将敏化的四个区域用特贝林素pH4.3,三巴氟胺pH 7.0,盐水pH 4.3或盐水pH 7.0注射。在注射相应溶液后,在诱导UVB致敏之后和15,30和60分钟之前和之后检查疼痛阈值。皮肤和深层组织的机械疼痛阈值分别通过拼针和压力距测量测量来确定。结果UVB-辐照降低了针刺和压力距离测量的机械疼痛阈值,证明了成功的晒伤性敏感性。皮下注射到致敏皮肤中的特对丁氨氨酸pH 7.0降低了通过针刺测量确定的所有测量时间点的敏化。通过注射三丁碱pH4.3,盐水溶液pH7.0或盐水溶液pH4.3,不降低致敏的针刺测量。此外,通过用压力距测量的任何注射液不会改变更深组织伤害者的敏化。结论类似于我们的细胞观测,也是β-肾上腺素能激动剂,如特许醛,可以降低皮肤中原发性神经元的敏化。我们以前在模型系统中显示的意义,β-肾上腺素能刺激不仅可以敏感,而且脱敏伤害者。我们的研究表明,如果注射到UVB致敏的皮肤中,也表明人类β-肾上腺素能激动剂脱敏。这表明除了血管收缩功能外,肾上腺素能激动剂的镇痛活性。

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  • 来源
    《European journal of pain :》 |2019年第1期|共9页
  • 作者单位

    Univ Clin Cologne Dept Anaesthesiol &

    Intens Care Med Cologne Germany;

    Hosp Zum Heiligen Geist GmbH Dept Pain Therapy Kempen Germany;

    Hannover Med Sch Dept Anaesthesiol &

    Intens Care Med Hannover Germany;

    Hannover Med Sch Dept Anaesthesiol &

    Intens Care Med Hannover Germany;

    Hannover Med Sch Dept Anaesthesiol &

    Intens Care Med Hannover Germany;

    Univ Clin Cologne Dept Anaesthesiol &

    Intens Care Med Cologne Germany;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 诊断学;
  • 关键词

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