摘要
目的 :观察败血症休克大鼠主动脉内膜、中膜和外膜一氧化氮合成途径的改变。方法 :雄性Wistar大鼠盲肠结扎并穿孔复制败血症休克模型 ,分别测定假手术组、早期休克组和晚期休克组大鼠主动脉内膜、中膜和外膜的亚硝酸盐 (NO-2 )含量、一氧化氮合酶 (NOS)活性及L -精氨酸 (L -Arg)转运 ;免疫组化染色检测诱导型一氧化氮合酶 (iNOS)在主动脉各层的分布。结果 :早期及晚期败血症休克大鼠主动脉内膜产生的NO-2 含量、NOS活性及L-Arg转运速率均低于假手术组 ,而中膜和外膜的NO-2 、NOS活性及L -Arg转运速率则显著高于假手术组 ,外膜增加的程度尤为显著。免疫组织化学染色显示 ,败血症休克时血管中膜和外膜尤其是外膜iNOS阳性染色明显较强。结论 :败血症休克时血管内膜NO合成受到抑制 ,而中膜和外膜NO合成显著增强 ,这一改变与休克状态下血管中L-Arg转运。
AIM: To observe the change of nitric oxide (NO) generation system in the vascular adventitia, media and intima in septic shock rats. METHODS: The septic shock model was made in rats by caecal ligation and puncture. The intima, media and adventitia of the rat aorta were separated. NO production (NO - 2) , nitric oxide synthase(NOS) activity and L-arginine (L-Arg) transport were measured, separately. Inducible NOS (iNOS) distribution was detected by immunohistochemistry. RESULTS: Both in early and late stage of septic shock, NO - 2 from the intima was decreased by 66.1% and 78.9%( P <0.01), while NO - 2 from the media was increased by 1.1 and 2.2 folds( P< 0.01), and the adventitia 9.6 and 18.6-fold ( P< 0.01), as compared with the sham group, respectively. The changes of NOS activity and the L-arginine transport in the intima, the media layer and the adventitia of the aorta in the septic shock rat paralleled with that of NO - 2 in these tissues. The results of iNOS immunohistochemistry showed that there were obviously positive staining in the media layer and adventitia, especially the adventitia of the rat aortas in septic shock, as compared with that in the sham control. CONCLUSIONS: During septic shock, NO production in the aortic intima was progressively suppressed. However, it was progressively increased in the aortic medial layer and adventitia, especially the adventitia with shock processes. These changes result from different changes of L-arginine transport, NOS activity and its expression in three layers of the aorta from the septic shock rat.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2003年第5期599-603,T003,共6页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目 (No .39970 2 95 )
