氯胺酮脑保护作用的可能机制

Protective mechanisms of ketamine on ischemia induced cerebral damage

众多研究显示，氯胺酮对脑缺血缺氧性损伤具有保护作用。主要通过调节神经细胞凋亡；与NMDA受体结合，抑制兴奋性氨基酸毒性及钙离子内流；抑制炎性因子生成和蛋白激酶表达等几个方面发挥脑保护作用。

Ketamine is a commonly used anesthetic agent, and is also the unique noncompetitive NMDA receptor antagonist used in clinic. Recently studies have shown that ketamine does not alter cerebral hemodynamics adversely when given to patients under mechanical ventilation and background anesthetics. More studies also shown ketamine has neuroprotective effects. The main mechanisms may involve in changing the expression of apoptosis-regulating proteins, inhibiting the toxicibility of excitatory amino acid, and decreasing Ca^2＋ influx by blockade of NMDA receptors activation. Ketamine can also inhibit proinflammatory cytokine production induced by tissue ischemia and affect the protein kinase phosphorylations related to cerebral ischemia. There are also some other mechanisms. The aim of our review is to summarize the possible neuroprotective mechanisms of ketamine.