脑性盐耗综合征的发病机制及钠代谢中枢的解剖位置  

Pathogenesis of cerebral salt wasting syndrome and anatomic localization of sodium metabolism regulator center

作　　者：徐志纯[1,2] 马书伟[2] 

机构地区：[1]福建医科大学第一临床医学院,福建福州350004 [2]厦门市第二医院神经外科,福建厦门361021

出　　处：《局解手术学杂志》2013年第1期55-57,共3页Journal of Regional Anatomy and Operative Surgery

摘　　要：目的探讨脑性盐耗综合征的发病机制及临床问题。方法 2007年7月至2012年7月治疗脑性盐耗综合征9例。依照患者补盐量与尿量有无直线回归关系将病例分为2组,对其补盐量、尿量、每日尿量/补盐量的均数做两样本t检验。结果 9例均治愈,其中6例补盐量与尿量有直线回归关系,P<0.05;3例补盐量与尿量无直线回归关系,P>0.05。有直线回归关系组与无直线关系组相比:补盐量前者大于后者(P<0.001);尿量前者大于后者(P<0.001);但2组单位补盐量所对应的尿量(尿量/补盐量)不相等(P>0.05)。结论脑性盐耗综合征患者补盐量与尿量的直线回归关系,补盐后肾脏排钠增加,因此,钠代谢中枢的解剖位置可能是以下丘脑为主,包括额叶、侧裂周围脑组织的广泛区域。Objective To investigate the pathogenesis and clinical problems of cerebral salt wasting syndrome.Methods Nine cases of cerebral salt wasting syndrome were treated from July 2007 to July 2012.Linear regression analysis of urine output and salt input was performed on these cases,and they were divided into two groups according to the analysis results.Independent-Samples t test was performed on the means of salt input,urine output and urine output/salt input of each group.Results All of the nine cases were cured,six cases of which has a linear regression relationship of salt input and urine output（P0.05） while the other three cases has not（P0.05）.Compared with the non-linear regression group,the linear regression group has more salt input（P0.001） and more urine output（P0.001）;but the means of urine output/salt input of two groups is not equal（P0.5）.Conclusion From the linear regression relationship of salt input and urine output in cerebral salt wasting syndrome,it was proved that urine output depends on salt input.The anatomic localization of sodium metabolism regulator center may be in hypothalamus as the primary,including the frontal lobe and the brain tissue around the lateral fissure.

关 键 词：脑性盐耗综合征 发病机制 钠代谢中枢 解剖定位 

分 类 号：R589.4[医药卫生—内分泌]