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.
出处
《急诊医学》
CSCD
1999年第3期160-161,共2页