利多卡因的脑保护机制

Cerebral protective mechanism of lidocaine

利多卡因具有脑保护作用,其机制与下列因素有关:阻断膜Na+-K+交换,ATP的消耗减少,因而减少自由基的产生,同时抑制缺血脑细胞K+外流及游离脂肪酸释放;抑制膜上电压依赖性Ca2+通道,减轻H2O2诱导的脂质过氧化反应;有效减轻缺血再灌注时神经细胞离子的紊乱,阻止细胞内Na+浓度的升高,降低突触前的谷氨酸释放;抑制线粒体的有氧代谢,降低线粒体内能量物质代谢速率,趋缓乳酸水平的升高,从而减轻细胞内乳酸的堆积,提高细胞对缺氧的耐受力;抑制缺血脑灌注后脑型肌酸激酶的释放,从而使脑缺血时的神经膜保持稳定;改善细胞渗透压和ATP的利用及Ca2+的清除等,从而起到保护神经的作用。

Recent studies have indicated that lidocaine possesses brain protection.The mechanisms are concerned with the following factors： blockade cell membrane Na^＋-K^＋ exchange and decrease consumption of adenosine triphosphate resulting in reducing free radical production,inhibiting out-flow of potassium ion and release of free fatty acids,inhibit voltage-dependent Ca^2＋channel in the cell membraneand abate lipid peroxidation reaction induced by hydrogen peroxide;abate cellula nervosa ionic derangement during ischemic-reperfusion and hamper increase of intra-cellular sodium and degrade release of presynaptic aminoglutaminic acid;inhibit aerobic metabolism and degrade energy and substance metabolism rate in mitochondrial leading to decreased lactic acid level,which results in abating intra-cellular lactic acid accumulation and elevating tolerance to hypoxia of cells;inhibit release of B-creatinkinase reperfusion after cerebral ischemic,to retain stabilization of neurolemmas in cerebral ischemia;adjust osmotic pressure in cells;improve utilization of adenosine triphosphate and clearance of calcium ion leading to nerve protection.