摘要
目的 :研究一氧化氮合酶 (NOS)抑制剂与严重烧伤大鼠体内NO产量、NOS表达以及平均动脉压(MAP)变化的关系。方法 :复制大鼠重症烧伤模型 ,检测应用非选择性NOS抑制剂L -NAME和选择性诱生型NOS(iNOS)抑制剂氨基胍 (AG)后大鼠血液中NO代谢产物 (NO- 2 /NO- 3)以及肺和十二指肠组织中神经型NOS(nNOS)mR NA的表达水平 ,同时测定各组大鼠的MAP。结果 :烧伤后大鼠血液中NO- 2 /NO- 3含量显著增高 ,L -NAME和AG都能抑制NO- 2 /NO- 3的升高 ,P <0 .0 1 ;烧伤后nNOS的mRNA表达在肺和十二指肠中均有不同程度升高 ,AG和L -NAME使nNOS表达增加 ,L -NAME作用更为显著 ,P <0 .0 1 ;烧伤后大鼠MAP略有上升 ,然后进行性下降 ,L -NAME组大鼠MAP显著升高 ,但于 3h后急剧下降 ,AG组大鼠MAP下降速度明显低于对照组。结论 :结构型NOS(cNOS)与iNOS在烧伤休克病理生理过程中的作用明显不同 ,iNOS活性过度增高与烧伤休克发病关系密切。
AIM: To identify the effects of nitric oxide synthase (NOS) inhibitor on NO production, expression of NOS and mean artery pressure (MAP) in rats with severe burns. METHODS: After administration of non-selective NOS inhibitor, L-NAME, and selective inducible NOS (iNOS) inhibitor, aminoguanidine (AG), to rats with severe burns, levels of NO - 2/NO - 3 in blood, mRNA expression of nerve NOS (nNOS) in lung and duodenum, MAP in each group were calculated. RESULTS: Levels of NO - 2/NO - 3 in blood of rats increased significantly post burn, which could be inhibited by L-NAME and AG, especially by L-NAME. Expression of nNOS mRNA in lung and duodenum of rats increased post burn, which could be enhanced by AG and L-NAME. MAP of rats decreased gradually post burn and administration of AG could slow down this process significantly. CONCLUSION: cNOS and iNOS could play different roles in the pathophysiology of burn shock. Over-expression of iNOS could be closely related to the pathogenesis of burn shock.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2003年第1期47-50,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目 (30 0 70 735)
