【摘要】 目的观察曲马多中毒死亡后人脑延髓孤束核和疑核中γ-氨基丁酸(gamma-amino butyric acid,GABA)A受体α1亚型(GABAAα1)和B受体1亚型(GABAB1)的表达变化,探讨曲马多中毒死亡的机制。方法应用免疫组织化学方法,观察比较曲马多中毒死亡人脑与非中毒原因死亡人脑延髓孤束核和疑核的GABAAα1和GABAB1的变化,并用图像分析系统进行分析。结果非中毒原因死亡人脑延髓孤束核和疑核有低水平的GABAAα1和GABAB1表达,曲马多中毒死亡人脑延髓孤束核和疑核的GABAAα1和GABAB1表达明显增加。结论曲马多中毒死亡的机制可能是由于人脑延髓孤束核和疑核GABAAα1和GABAB1表达增加所致的呼吸抑制。更多还原

【Abstract】 Objective To observe the expression of GABAA receptor α1(GABAAα1) and GABAB receptor 1(GABAB1) in human medulla oblongata solitary nucleus and ambiguous nucleus due to tramadol-induced death.Methods GABAAα1 and GABAB1 were detected by immunohistochemical SP method in tramadol-induced death group and control group.All results were evaluated by images analysis system.Results Low expression of GABAAα1 and GABAB1 were detected in solitary nucleus and ambiguous nucleus in the control brain tissue.In cases of tramadol-induced death,the expression of GABAAα1 and GABAB1 significantly increased.Conclusion The mechanism of tramadol intoxication death could be caused by respiratory depression induced by over-expression of GABAAα1 and GABAB1 in medulla oblongata solitary nucleus and ambiguous nucleus.更多还原