持续性钠电流与细胞缺血缺氧  

Persistent Sodium Current and Cellular Ischemia and Hypoxia

作　　者：江炜炜[1] 柯开富[2] 

机构地区：[1]南京医科大学附属南京脑科医院神经内科,210029 [2]南通大学附属医院神经内科,226001

出　　处：《国外医学（脑血管疾病分册）》2005年第10期788-792,共5页Foreign Medical Sciences Cerebrovascular Diseases

摘　　要：持续性钠电流由可兴奋细胞膜上某些对河豚毒素敏感的电压依赖性钠通道持续开放产生,随着膜片钳技术的广泛应用,对其了解逐渐深入。近年来发现,持续性钠电流与细胞缺血缺氧关系密切。缺血缺氧时,持续性钠电流的幅度增大导致细胞内Na+浓度增高,进而引起细胞内Ca2+浓度增高、细胞外谷氨酸浓度增高以及细胞兴奋性改变,最终导致细胞不可逆性损伤甚至死亡。目前认为,持续性钠电流增大是缺血缺氧时细胞损伤的一种早期基础性病理学过程。Persistent sodium current can be generated by some tetradotoxin-sensitive voltagedependent sodium channels on the excitable cell membranes, which continue to open for a long time. With the wide use of patch-clamp technique, the understanding of persistent sodium current is gradually developing in depth. In recent years, it has been found that persistent sodium current is closely associated with cellular ischemia and hypoxia. During cellular ischemia and hypoxia, the amplitude of persistent sodium current increases and thus results in the increase of intracellular concentrations of Na^＋ and Ca^2＋, the increase of extracellular glutamac acid concentration, as well as the changes of cell excitability, and ultimately results in cell irreversible injury and even death. It is considered that the increase of persistent sodium current is an early fundamental pathological process in cell injury during ischemia and hypoxia.

关 键 词：持续性钠电流 缺血状态 缺氧状态 钠通道 膜片钳 

分 类 号：R741[医药卫生—神经病学与精神病学]