中文摘要：

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。

英文摘要：

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.