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目的 阐明羟基自由基（·ＯＨ） 在脑内痛觉信息调控中的作用及机制。方法 采用小鼠温浴缩尾模型（ＴＩＴ） 、热板模型（ＨＰ） 、扭体模型（ＡＡ） 及福尔马林模型（Ｆｏｒ） 等多种经典模型，将·ＯＨ反应液直接注入小鼠体内，观察小鼠痛阈的变化；并使用·ＯＨ清除剂ＤＭＳＯ 观察内、外源性·ＯＨ对小鼠痛阈的影响；用Ｃａ２＋ 阻滞剂及ＮＭＤＡ 受体拮抗剂分析·ＯＨ的作用与Ｃａ２＋ 、ＮＭＤＡ 受体的关系；测定疼痛过程中小鼠脊髓、脑、血中ＰＧｓ 含量的变化，分析·ＯＨ作用与ＰＧｓ 间关系。结果 外源性·ＯＨ有中枢致痛敏作用；内源性·ＯＨ部分参与炎性痛反应；疼痛过程中出现细胞内Ｃａ２＋ 增高、ＮＭＤＡ 受体的激活。结论 内、外源性·ＯＨ在中枢痛觉信息调控中具有重要作用；机制涉及细胞内高钙、ＮＭＤＡ 受体的激活等。
Objective To elucidate the role and mechanism of hydroxyl radical (· OH) in the regulation of intracerebral pain information. Methods The mouse hot bath tail model (TIT), hot plate model (HP), writhing model (AA) and Formalin model (For) and other classic models, the · OH reaction solution directly into mice The changes of pain threshold in mice were observed. The effects of exogenous OH and OH on the pain threshold of mice were observed by using OH scavenger DMSO. The effects of OH and Ca2 + blockers and NMDA receptor antagonists on Ca2 + , And NMDA receptors. To determine the changes of PGs in the spinal cord, brain and blood of mice during pain, the relationship between · OH and PGs was analyzed. Results Exogenous · OH had central pain sensitization; endogenous · OH partially involved in inflammatory pain reaction; intracellular Ca2 + increased and NMDA receptor activation occurred during pain. Conclusions, exogenous · OH plays an important role in the regulation of central pain information; the mechanism involves the intracellular high calcium and NMDA receptor activation.