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目的观察新生大鼠内毒素休克时血清TNF-α和NO的动态变化以及与心肌细胞损害的关系,探讨地塞米松(DXM)对心肌的保护作用。方法健康7 d Wistar大鼠17只,随机取9只作实验前基础值组,余108只随机分成对照组、休克组(LPS 5 mg/kg)及治疗组(LPS 5 mg/kg+DXM 5 mg/kg)。各组于注射LPS前(0 h)及注射后2,4,6,24 h分别断头取血并留取心脏组织。双抗夹心ELISA方法测定血清TNF-α浓度,硝酸盐还原酶法测定血清NO浓度,以透射电镜观察心肌超微结构改变。结果①休克组TNF-α于注射LPS2 h达高峰,6 h后下 降到对照组水平。注射LPS 2 h后,DXM组TNF-α高于对照组(P<0.05),但明显低于休克组(P<0.05);注射LPS 4 h,DXM组TNF-α含量低于休克组(P<0.05),但与对照组差异无显著性(P>0.05)。LPS注射后6 h起,3组问TNF-α差异均无显著性(P>0.05)。②休克组血清NO从注射LPS 2 h起升高(P<0.01),24 h达高峰(P<0.01);从注射LPS 2 h起,DXM组血清NO均低于同时间点休克组(P<0.01)。③心肌超微结构改变:休克组于注射LPS 6 h心肌细胞少数线粒体有空泡变性,24 h出现心肌纤维断裂、大量线粒体空泡变性、坏死。而DXM组在注射LPS24 h仅少数线粒体有空泡变性,心肌纤维完整。结论内毒素休克新生大鼠通过释放炎症介质损害心肌组织,DXM通过抑制炎症介质
Objective To observe the dynamic changes of TNF-α and NO in endotoxic shock and the relationship between TNF-α and NO in cardiomyocytes and to explore the protective effect of DXM on myocardium. Methods Seventeen healthy Wistar rats were randomly divided into control group, shock group (LPS 5 mg / kg) and treatment group (LPS 5 mg / kg + DXM 5) mg / kg). Each group was decapitated before the injection of LPS (0 h) and 2,4,6,24 h after injection of blood and heart tissue. The concentration of serum TNF-α was measured by double-antibody sandwich ELISA. The concentration of serum NO was determined by nitrate reductase method. The ultrastructure of myocardium was observed by transmission electron microscope. Results ① In shock group, TNF-α peaked at 2 h after injection of LPS, and then dropped to the level of control group 6 h later. The TNF-α level in DXM group was significantly lower than that in shock group (P <0.05) at 2 h after LPS injection, but was significantly lower in DXM group than that in shock group (P <0.05) <0.05), but no significant difference with the control group (P> 0.05). There was no significant difference in TNF-α between the three groups 6 h after LPS injection (P> 0.05). (2) Serum NO in shock group increased from 2 h after LPS injection (P <0.01) and peaked at 24 h (P <0.01); NO levels in DXM group were lower than those in shock shock group <0.01). ③ myocardial ultrastructure changes: Shock group at 6 h after LPS injection of myocardial mitochondria mitochondria degeneration, myocardial fibrosis 24 h broke, a large number of mitochondrial degeneration and necrosis. In the DXM group, only a few mitochondria were vacuolar degeneration in 24 h after LPS injection, and the myocardial fibers were intact. Conclusion Endotoxic shock in neonatal rats through the release of inflammatory mediators damage myocardial tissue, DXM by inhibiting inflammatory mediators