三七花总皂苷对大鼠离体胸主动脉的舒张作用及其机制

Vasodilatory effects of flower of Panax notoginseng saponins on rat aorta

目的研究三七花总皂苷对大鼠离体胸主动脉的舒张作用,探讨其可能机制。方法提取分离得到三七花总皂苷,利用指纹图谱说明其成分;分离SD大鼠胸主动脉,采用离体血管环实验,观察三七花总皂苷对血管环基础状态,高浓度K+溶液预收缩及苯肾上腺素(phenylephrine,PE)预收缩引起的舒缩功能的反应,并结合不同抑制剂处理,探讨三七花总皂苷作用血管环的可能机制。结果累计浓度的三七花总皂苷对基础状态血管无明显影响;对高浓度K+预收缩的血管环对内皮完整最大舒张率可达23.6%;对PE预收缩的血管环在有无内皮完整差异有统计学意义,三七花总皂苷内皮完整的情况下最大舒张率可达55.51%;无钙液与皂苷培育的血管环对PE预收缩有明显的收缩抑制作用;对一氧化氮合酶抑制剂L-NAME孵育血管环后能明显抑制三七花总皂苷扩血管的作用;对环氧合酶抑制剂吲哚美辛孵育血管环后能明显抑制三七花总皂苷扩血管的作用。结论三七花总皂苷引起离体大鼠胸主动脉的舒张作用途径:内皮依耐性舒张主要与激活氧化氮合酶途径与激活环氧合酶途径有关。

Aim To investigate the vasorelaxation effects of saponins from flower of Panax notoginsen on the isolated thoracica aorta ,and to explore its possible mechanism.Methods Total saponins were extracted and high phase liquid chromatography was utilized to describe saponins ingredients;SD rat thoracic aortas were isolated.In vitro vascular ring experiment was used to observe,basal state of saponins on vascular ring,and high concentrations of K＋solution pre-con-traction and phenylephrine （PE ） pre-contraction caused by systolic and diastolic function of the re-sponse.And different inhibitors were combined to ex-amine the possible mechanism of notoginsenoside in vascular ring.Results Cumulative concentration of saponins had no significant effect on the basis of state vessels,but had significant effect on endothelium-in-tact aortic （MAX Relaxation 23.6%） rings pre-con-tracted by high concentrations of K＋;endothelium and endothelial aortia had significant effect on PE pre-con-traction, and endothelium MAX relaxation was 55.5 1%.Calcium-free solution and saponin cultivated aortic rings significantly inhibited pre-contraction.Af-ter nitric oxide synthase inhibitor L-NAME and indom-ethacin incubating vascular ring ,it could significantly inhibited vasodilatory effect of saponin.Conclusion Saponins have concentration dependent diastolic func-tion on rat thoracic aorta,and its main ways cause vas-odilation.Endothelial dependent diastolic function is related to activation of nitric oxide synthase and cy-clooxygenase pathway.