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目的探讨黄芪对过氧亚硝酸盐阴离子(ONOO-)导致的血管反应性异常的影响。方法 32只SD大鼠随机分为2组,正常对照组与黄芪灌胃组,每组16只。大鼠喂养4周后处死,取胸主动脉,制备离体血管环标本。每组大鼠血管随机分为不同处理组(ONOO-组、未处理组)孵育。完成孵育后采用大鼠离体主动脉环灌流模型观察2组大鼠血管对苯肾上素(PE)/乙酰胆碱(Ach)诱导的收缩/舒张反应性的变化。结果正常对照组不同处理血管在PE的作用下收缩反应性均呈浓度依赖性增高;在高浓度(10、100μmol/L)时,ONOO-处理组血管对PE的最大收缩力明显高于未处理组(P均<0.05);2组血管在Ach的作用下舒张反应性均呈浓度依赖性增高,在高浓度(100μmol/L)时,ONOO-处理组血管对Ach的最大舒张率明显低于未处理组(P<0.05)。在黄芪灌胃ONOO-处理组与未处理组大鼠血管上述改变均无明显差异(P>0.05)。表明ONOO-导致的血管舒缩功能异常可以被黄芪改善。结论黄芪可改善ONOO-导致的血管反应性异常,因此对血管功能具有保护作用。
Objective To investigate the effect of Radix Astragali on the vascular reactivity induced by peroxynitrite (ONOO-). Methods Thirty-two Sprague-Dawley rats were randomly divided into two groups. Normal control group and Astragalus gavage group were given 16 rats in each group. Four weeks after the rats were sacrificed, the thoracic aorta was taken and isolated vascular rings were prepared. The blood vessels in each group were randomly divided into different treatment groups (ONOO-group, untreated group). After completing the incubation, the isolated rat aortic rings were used to observe the change of contraction / relaxation response induced by phenylephrine / acetylcholine (Ach) in the blood vessels of the two groups. Results Compared with the control group, the contractile responses of the vessels in the normal control group increased in a concentration-dependent manner. At the concentrations of 10 and 100 μmol / L, the maximal contractile force of PE on the ONOO-treated group was significantly higher than that of the untreated (All P <0.05). The relaxation responses of Ach in both groups were increased in a concentration-dependent manner. At the concentration of 100 μmol / L, the maximal relaxation rate of Ach in ONOO- Untreated group (P <0.05). There was no significant difference in the above-mentioned changes of blood vessel between ONOO-treated group and untreated group (P> 0.05). That ONOO-induced vasomotor dysfunction can be improved by Astragalus. Conclusion Astragalus can improve ONOO- -induced vascular reactivity abnormality, and therefore has a protective effect on vascular function.