NO在血管内皮细胞损伤中的标志作用  

The marker Role of nitric oxide in the damage of vascular endothelial cell

作　　者：杨春华[1] 林水金[2] 杨映波 冯素珍[2] 

机构地区：[1]广州军区总医院ICU,广州510010 [2]第三军医大学创伤科

出　　处：《急诊医学》1999年第3期160-161,共2页

摘　　要：目的 :探讨一氧化氮 (NO)在血管内皮细胞 (VEC)损伤中的作用。方法 :利用创伤失血性休克造成兔VEC损伤 ,检测创伤前、创伤后 6小时及 1、 3、 7天外周血内皮素 (ET)及NO含量 ,并观测VEC超微结构的改变。结果 :伤后 6小时及第 1天 ,外周血ET、NO含量同步显著升高 ,而且NO含量高峰较ET提前出现。伤后第 3、 7天 ,外周血ET、NO含量同步显著下降。VEC超微结构于伤后 6小时无改变 ,伤后第 1天VEC超微结构损伤轻微 ,伤后第 3、 7天损伤严重。结论 :1.NO与ET早期同步升高 ,可拮抗ET升高引起的血管痉挛 ,改善组织血供。2 .NO作为VCE损伤标志物较ET更为敏感。Aim:To explore the marker role of nitric oxide(NO)in the damage of vascular endothelial cell(VEC).Methods:A traumatic low volume shock model of rabbit was made and then examined the concentration of endothelin(ET)and NO in the peripheral blood before and 6 h or 1、3、7 days after trauma.The ultrastructure of VEC of rabbit kidney was also observed at the same time.Results:The concentration of ET and NO in the peripheral blood increased obviously 6 h or 1 day after trauma and decreased rapidly 3 or 7 days after wards.But the peak concentration of NO came up earlier than that of ET.The ultrastructure of VEC did not show any damage 6 hours after trama,but showed slight damage 1 day after wards,and sevese damage 3、7 days after trauma.Conclusion:1.The early synchronous in crease of NO and ET could antagonize the vascular spasm resulting from elevation of ET.2.NO is more sensitive as a marker of VEC than ET.

关 键 词：内皮素 一氧化氮 血管内皮细胞 标志作用 损伤 

分 类 号：R543[医药卫生—心血管疾病] R361.3[医药卫生—内科学]