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作 者:金晓红[1] 杨建平[1] 成浩[1] 王丽娜[1] 嵇富海[1]
机构地区:[1]苏州大学附属第一医院麻醉科,江苏苏州215006
出 处:《药物生物技术》2010年第5期404-407,共4页Pharmaceutical Biotechnology
基 金:国家自然科学基金资助课题(No.30872442);江苏省卫生厅基金资助课题(No.H200855);江苏省卫生厅基金资助课题(No.H200917)
摘 要:通过大鼠结直肠内充气扩张(CRD)的内脏痛模型,探讨脊髓水平α2-肾上腺素受体在异丙酚抗内脏伤害效应机制中的作用。实验采用成年雄性SD大鼠,应用免疫组织化学的方法,观察鞘内预先注射α2肾上腺素受体拮抗剂育亨宾后异丙酚CRD大鼠脊髓L6~S1节段Fos蛋白表达的变化。结果显示结直肠充气扩张产生内脏伤害刺激后大鼠脊髓L6~S1节段Fos蛋白的表达显著增加,腹腔注射催眠剂量异丙酚(100mg/kg)则明显减少大鼠脊髓L6~S1节段Fos蛋白的表达。而预先鞘内注射育亨宾(15μg/只)能部分逆转异丙酚的这一抗内脏伤害效应。证明异丙酚的抗内脏伤害效应的作用机制与脊髓水平α2肾上腺素受体的激活有关。Using a visceral pain model by colorectal distension(CRD)in rats to explore the effects of α2-adrenoceptors in spinal cord in response visceral analgesia of propofol,the experiments were performed on adult male Sprague-Dawley rats and the visceral nociceptive stimulus was generated by a noxious colorectal distention with a colorectal ballonet.Rats were treated with vehicle or yohimbine 15μg/rat intrathecal pre-injection and vehicle or propofol 100mg/kg intraperitoneal injection.Then a noxious CRD(80mm Hg,20min)was given except the control group.Each lumbosacral spinal cord segment(L6~S1)was removed for observing the difference of Fos expression in lumborsacral spinal cord.Experiment results showed that Fos expression in lumborsacral spinal cord increased significantly after a noxious CRD but decreased when a hypnotic dose of propofol was administered intraperitoneally.This indicated that propofol had antinociceptive effect on visceral nociception.Otherwise,yohimbine pretreatment intrathecally partially reversed this effect of propofol.This research indicates that spinal cord α2-ardenoceptors are involved in the visceral analgesic mechanism of propofol.
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