地佐辛
瑞芬太尼
痛觉过敏
医学
麻醉
兴奋剂
药理学
内科学
伤害
受体
止痛药
异丙酚
作者
Jie Zhou,Fengsheng Qi,Zhengqiang Hu,Lejun Zhang,Zigang Li,Zaijie Jim Wang,Huifang Tang,Zhijun Chen
标识
DOI:10.1016/j.ejphar.2019.172882
摘要
Remifentanil, ultra-short-acting μ-opioid receptor agonist, has the greatest advantage in analgesia but could increase postoperative pain scores and induces postoperative hyperalgesia. Dezocine is a mixed opioid receptor partial agonist/antagonist and has been used for postoperative hyperalgesia management in clinical patients,but the potential molecular mechanism is still unclear. Ca2+/calmodulin-dependent protein kinase Ⅱ(CaMKⅡ) has been reported involved in remifentanil-induced hyperalgesia (RIH) in previous studies, but the relationship between CaMKⅡ and dezocine in RIH is still unclear. To investigate the mechanism of dezocine in RIH, we used a remifentanil induced postoperative hyperalgesia (RIPH) in incisional pain model of mouse. We subcutaneously infused remifentanil (40 μg/kg) to induce postoperative hyperalgesia. Dezocine (1.5 mg/kg, 3.0 mg/kg, and 6.0 mg/kg) was infused subcutaneously with remifentanil using the apparatus pump for 30 min. Paw withdrawal thermal latency (PWTL) and paw withdrawal mechanical threshold (PWMT) were used to assess thermal hyperalgesia and mechanical allodynia. Western blotting analysis and immunohistochemistry analysis were used to assess the expression of phosphorylated CaMKⅡα (p-CaMKⅡα) in somatosensory cortex, hippocampus and spinal cord. Subcutaneous infusion of remifentanil enhanced postoperative pain induced by surgical incision and increased PWTL and PWMT. Dezocine dose-dependently decreased the PWTL and PWMT in RIPH model. Correlating with behavioral effects, dezocine inhibited remifentanil-induced up-regulation of p-CaMKⅡα expression in somatosensory cortex, hippocampus and spinal cord. Dezocine could attenuate RIPH by suppressing p-CaMKⅡα.
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