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作 者:孙和勇 张刚利[1] Sun Heyong;Zhang Gangli(Department of Neurosurgery,the Fifth Clinical Medical College of Shanxi Medical University,Shanxi Provincial People’s Hospital,Taiyuan 030012,China)
机构地区:[1]山西医科大学第五临床医学院,山西省人民医院神经外科,太原030012
出 处:《中华实验外科杂志》2023年第12期2690-2696,共7页Chinese Journal of Experimental Surgery
基 金:山西省自然科学基金面上项目(202203021211060)。
摘 要:脑水肿是神经系统疾病患者最常出现的病理生理状态,导致颅内压增高甚至发生脑疝,最终导致不良预后。渗透性脱水是缓解脑水肿的一线治疗方案,常用脱水剂有甘露醇、高渗盐水(HS)、甘油果糖等。高渗盐水除了因高渗透压导致的脱水作用外,还通过其他机制发挥作用。本文总结了高渗盐水治疗脑水肿的非渗透性分子机制,主要包括下调水通道蛋白-4(AQP4)和离子通道蛋白Na-K-Cl共转运体1(NKCC1),保护血脑屏障(BBB)完整性,调节小胶质细胞向M2抗炎表型极化,减轻反应性星形胶质细胞激活,减少中性粒细胞的炎性浸润,减轻氧化应激损伤,以及改善凝血纤溶平衡。以上机制为HS的临床应用提供了理论依据。Brain edema is the most common pathophysiological state in patients with nervous system diseases,which leads to increased intracranial pressure and even cerebral hernia,resulting in poor prognosis.Osmotic dehydration is a first-line treatment for relieving brain edema.The commonly used dehydrating agents include mannitol,hypertonic saline(HS),glycerol fructose and so on.In addition to dehydration caused by high osmotic pressure,hypertonic saline also plays a role through other mechanisms.This paper summarized the non-permeable molecular mechanism of hypertonic saline in the treatment of brain edema,including down-regulating aquaporin-4(AQP4)and ion channel protein Na-K-Cl cotransporter 1(NKCC1),protecting the integrity of blood-brain barrier(BBB),regulating the polarization of microglia to M2 anti-inflammatory phenotype,reducing the activation of reactive astrocytes,reducing inflammatory infiltration of neutrophils,reducing oxidative stress injury,and improving the balance of coagulation and fibrinolysis.These mechanisms provide a theoretical basis for the clinical application of HS.
关 键 词:脑水肿 颅内高压 高渗盐水 非渗透性分子机制 综述
分 类 号:R742[医药卫生—神经病学与精神病学]
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