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目的:研究环维黄杨星D对大鼠胸主动脉去内皮血管环的舒张作用并探讨其机制。方法:采用氯化钾(KCl)或去氧肾上腺素(PE)预收缩血管,观察环维黄杨星D(10~600μmol/L)对大鼠胸主动脉去内皮血管的舒张作用;血管与600μmol/L环维黄杨星D预孵育后,观察其对KCl或PE收缩血管作用的影响;观察环维黄杨星D对不同钾离子通道阻断剂的血管反应性的影响;观察环维黄杨星D对CaCl_2收缩去内皮血管环的作用以及对PE产生的瞬时性收缩和加入CaCl_2后的持续性收缩的作用。结果:在给药浓度范围内(10~600μmol/L),环维黄杨星D能非内皮依赖性舒张由KCl和PE预收缩的大鼠胸主动脉血管环;600μmol/L环维黄杨星D与血管预孵育亦可明显抑制KCl或PE诱导的血管收缩;4-AP、Gly或TEA与血管环预孵育后,对600μmol/L环维黄杨星D舒张PE预收缩血管环的作用均没有影响;不同浓度(100、300和600μmol/L)的环维黄杨星D与血管环在无钙K-H液中预处理后,可以剂量依赖地抑制CaCl_2的浓度-效应曲线;300μmol/L环维黄杨星D与血管环在无钙K-H液中预处理后,可以显著抑制PE产生的瞬时性收缩以及加入CaCl_2后的持续性收缩。结论:环维黄杨星D对大鼠离体胸主动脉去内皮血管的舒张作用呈剂量依赖性,其对血管的舒张作用机制可能不涉及钾离子通道的活化,抑制血管平滑肌细胞的外钙内流和内钙释放作用可能参与了环维黄杨星D的舒血管机制。
OBJECTIVE: To investigate the vasodilation effect of cyclophosphamide D on the thoracic aorta in rats and its mechanism. Methods: Premature contraction of blood vessels was induced by potassium chloride (KCl) or phenylephrine (PE). The vasodilatation of the thoracic aorta in rats was observed by cyclophosphamide D (10 ~ 600μmol / L) / L-ring pretreatment of vimentin D to observe its effect on KCl or PE contraction of blood vessels; observation of cyclophosphamide D on the different potassium channel blockers of vascular reactivity; observe the ring Weiyang star D On CaCl 2 contraction to the role of the endothelium and the ring of PE produced by the transient contraction and the role of sustained contraction after addition of CaCl_2. Results: In the concentration range of administration (10 ~ 600μmol / L), cyclovirobuxine D could vasorelate the thoracic aorta rings of rats pre-contracted by KCl and PE without endothelium-dependent relaxation; Preincubation with vasoconstrictors also markedly inhibited KCl or PE-induced vasoconstriction. Preincubation with 600 μmol / L cyclophosphamide D did not affect the effect of pre-contracting vascular rings with 4-AP, Gly or TEA and vascular rings (100, 300 and 600μmol / L) of cyclophthiazovin D and vascular ring in calcium-free KH solution pretreatment can inhibit the dose-dependent CaCl2 concentration-effect curve; 300μmol / L ring Wickerman D and vascular rings in calcium-free KH solution pretreatment, can significantly inhibit the transient contraction of PE and sustained after the addition of CaCl 2 contraction. CONCLUSION: Cyclovirobuxine D has a dose-dependent effect on the vasorelaxation of isolated rat thoracic aorta in vitro. The mechanism of its vasodilatation may not be related to the activation of potassium channel and the inhibition of extracellular calcium in vascular smooth muscle cells Flow and internal calcium release may be involved in the vasodilator mechanism of cyclovirobuxine D.