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目的:研究丹酚酸B(salvianolic acid B,Sal B)对离体大鼠胸主动脉收缩张力的作用及其机制探讨。方法:SD大鼠,采用大鼠离体胸主动脉灌流模型,通过累积加药法加入Sal B使终浓度递增为1×10-8,1×10-7,1×10-6,1×10~(-5),1×10~(-4)mol·L~(-1),观察血管张力的变化,观察1×10~(-5),1×10~(-4)mol·L~(-1)Sal B对去甲肾上腺素(NE)和氯化钾(KCl)预收缩的胸主动脉环收缩张力的影响。结果:Sal B对内皮完整和内皮损伤的离体大鼠主动脉环基础张力的作用不明显;Sal B对NE预收缩的血管环有明显舒张作用,但对KCl预收缩的血管环无舒张作用;用一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(L-NAME)和环氧酶抑制剂吲哚美辛(Indo)处理血管后,对Sal B舒张血管效应阻断作用不明显,使用电压依赖性的K+通道阻断剂4-AP,Ca2+敏感性的K+通道阻断剂四乙胺(TEA)以及ATP敏感性的K+通道阻断剂格列苯脲处理后,对Sal B舒张血管效应的阻断作用不明显,使用β受体阻断药普萘洛尔处理后,对Sal B舒张血管效应的阻断作用亦不明显;而Sal B对Ca2+引起的收缩有抑制作用,抑制内钙收缩作用比外钙收缩作用更强。结论:Sal B舒张血管作用机制可能与阻断受体依赖性钙通道、电压依赖性钙通道引起的外钙内流和阻断三磷酸肌醇(IP3)受体引起的内钙释放有关,而与NO-鸟苷酸环化酶途径,环氧合酶途径,K+通道和β受体无关。
Objective: To investigate the effect and mechanism of salvianolic acid B (Sal B) on contractile tension of isolated thoracic aorta in rats. Methods: Sprague-Dawley rats were used in a rat thoracic aorta perfusion model. Sal B was added by cumulative dosing method to increase the final concentration to 1 × 10-8, 1 × 10-7, 1 × 10-6, 1 × The changes of vascular tone were observed after treatment with 10 ~ (-5), 1 × 10 ~ (-4) mol·L ~ (-1) Effects of L ~ (-1) Sal B on contractile tension of thoracic aorta rings pre-contracted by norepinephrine (NE) and potassium chloride (KCl). Results: Sal B had no obvious effect on the basic tension of isolated aortic rings of rats with endothelial integrity and endothelial injury. Sal B had a significant relaxation effect on NE pre-contracted vascular rings but no relaxation effect on pre-contracted vascular rings of KCl ; The nitric oxide synthase inhibitor L-NAME and the epoxide enzyme inhibitor indomethacin (Indo) treatment of blood vessels, vasodilator Sal B vasodilatation effect was not obvious , The K (superscript +) channel blocker 4-AP, the Ca2 + -sensitive K + channel blocker tetraethylamine (TEA) and ATP-sensitive K + channel blocker glibenclamide were used to treat Sal B The blocking effect of vasodilatation was not obvious, and the blockade effect of Sal B on vasodilatation was not obvious after using propranolol, a blocker of β-receptor. Sal B inhibited the contraction induced by Ca2 + Inhibition of calcium contraction than external calcium contraction stronger. CONCLUSIONS: The mechanism by which Sal B relaxes the blood vessels may be related to blockade of receptor-dependent calcium channels, extracellular calcium influx induced by voltage-dependent calcium channels and blockade of intracellular calcium release induced by the inositol 1,4,5triphosphate (IP3) receptor, whereas It has nothing to do with NO-guanylate cyclase pathway, cyclooxygenase pathway, K + channel and beta-receptor.