摘要
缺血性脑血管病是常见病、多发病,其致残率和死亡率均高,严重影响着人类的身体健康和生活质量。当脑缺血缺氧时,神经元会出现损伤和死亡。现有大量研究证明α2-肾上腺素受体激动剂能保护大脑神经元免受缺血/再灌注的损伤,但其发挥神经保护作用的确切机制尚不完全清楚,可能与α2-肾上腺素受体的激活有关。右旋美托嘧啶(dexmedetomidine)是一种高选择性的α2-肾上腺素受体激动剂,具有一定的神经保护作用。本文就缺血性脑血管病病理生理演变过程、右旋美托嘧啶的分子药理学及其发挥神经保护作用的机制作一综述。
Ischemic cerebrovascular disease is a common and frequently encountered disease with high disability and mortality rates,and has severe effects on human＇s health and quality of life. Cerebral hypoxic ischemia leads to an increase in the number of damaged or dead neurons. Recent studies have provided considerable evidence that alpha 2-adrenergic agonists can protect the brain neuron from cerebral ischemia/reperfusion injury. However,the exact mechanisms of this protection remain unknown. Activation of the alpha 2-adrenergic receptor may be involved. Dexmedetomidine is a highly selective agonist of the alpha 2-adrenergic receptors with neuroprotective effects. This article reviews the pathophysiological process of ischemic cerebrovascular disease,the molecular pharmacology and the neuroprotective mechanisms of dexmedetomidine.
出处
《神经药理学报》
2011年第5期49-55,共7页
Acta Neuropharmacologica
基金
国家自然科学基金青年科学基金项目(No.81100873)
湖北省卫生厅青年科技人才项目(No.QJX2012-27)
宜昌市科学技术研究与开发项目(No.A01301-02)
