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目的:探讨复方夏枯草活性部位(AFCP)对大鼠离体胸主动脉的作用及其可能的机制。方法:采用离体大鼠胸主动脉张力实验,经生物信号采集与分析系统测定血管环张力的变化,观察AFCP的舒张血管作用。结果:AFCP(100~500μg·ml-1)能显著降低苯肾上腺素(PE,1μmol·L-1)引起的血管收缩,对内皮完整和去内皮血管均有(75%±8%)舒张作用。AFCP的舒血管作用不受一氧化氮合酶抑制药L-NNA、岛苷酸环化酶抑制药MB、钾通道阻滞药TEA和格列苯脲的影响。在无钙K-H液中AFCP(300μg·ml-1)可使Ca Cl2的量效曲线下移且使PE的最大收缩幅度降低。结论:AFCP够浓度依赖性舒张大鼠胸主动脉,其舒张血管作用无内皮依赖性。其作用机制可能与抑制细胞内钙离子释放和细胞外钙离子内流有关,与NO途径、前列环素生成和钙激活的钾通道无关。
Objective: To investigate the effect of AFCP on rat isolated thoracic aorta and its possible mechanism. Methods: Isolated rat thoracic aorta tension test, the biosignal acquisition and analysis system to measure changes in vascular ring tension to observe the role of AFCP relaxation of blood vessels. Results: AFCP (100 ~ 500μg · ml-1) could significantly reduce the vasoconstriction induced by phenylephrine (PE, 1μmol·L-1) and had a relaxation effect of (75% ± 8%) on endothelial integrity and endothelium . The vasodilator effect of AFCP was not affected by the nitric oxide synthase inhibitor L-NNA, the inhibitor of the island glycosidase cyclooxygenase MB, the potassium channel blocker TEA and glibenclamide. AFCP (300μg · ml-1) in Ca-free K-H solution could down-shift the dose-response curve of CaCl 2 and decrease the maximum contraction of PE. Conclusion: AFCP is able to relax the thoracic aorta in a concentration-dependent manner without any endothelium-dependent vasodilation. Its mechanism of action may be related to the inhibition of intracellular calcium release and extracellular calcium influx, not with the NO pathway, prostacyclin production and calcium-activated potassium channels.