Na^＋，K^＋-ATP酶与脑缺血

Na^＋,K^＋-ATPase and cerebral ischemia

Na^＋,K^＋-ATP酶的基本功能是维持真核细胞膜内外Na^＋-K^＋电化学梯度平衡,后者为维持细胞渗透压、调节细胞体积和维持可兴奋细胞膜静息电位所必需.Na^＋，K^＋-ATP酶活性的维持在神经元神经递质的摄取和Ca^2＋外流中起着重要作用.脑缺血后,Na^＋，K^＋ -ATP酶活性降低及功能异常参与缺血性脑损伤过程.缺血预处理通过维持缺血后Na^＋，K^＋ -ATP酶活性而诱导缺血耐受.强心甾类固醇和胞二磷胆碱可通过提高Na^＋，K^＋-ATP酶活性对脑缺血发挥神经保护效应.

The basic functions of the Na^＋/K^＋ -ATPase is to maintain the balance of the Na^＋/K^＋ electrochemical gradient. The latter is indispensable for maintaining cell osmotic pressure, regulating cell volume, and maintaining excitable membrane resting potential. The maintenance of the Na^＋/K^＋-AIPase activity plays the important roles in neurotransmitter uptake in neurons and Ca^2 ＋ efflux. The decreased Na^＋/K^＋ -ATPase activity and dysfunction participate in the process of ischemic brain injury after cerebral ischemia. Ischemic preconditioning induces ischemic tolerance by maintaining the Na^＋/K^＋ -ATPase activity after ischemia. Cardiotonic steroids and citicoline may play a neuroprotective effect on cerebral ischemia by improving the Na^＋/K^＋-ATPase activity.