摘要
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 investigated the effects and mechanism of salvianolic acid B（ Sal B） on vasorelaxation of isolated thoracic aorta in rats. Method： SD rats were used to establish isolated thoracic aorta perfusion models,and the cumulative dosing method was used to add Sal B to make final concentrations of 1 ×10^-8,1 × 10^-7,1 × 10^-6,1 × 10^-5,1 × 10^-4mol·L^-1. The vascular tension changes were observed,and the effects 1 × 10^-5,1 × 10^-4mol·L^-1Sal B on the constriction of norepinephrine（ NE） and KCl preconstricted thoracic aorta were observed in rats. Result： The effect of Sal B on the basal tonus in isolated aortic rings in rats with endothelial integrity or endothelial injury was not so significant. Sal B dependently caused relaxation in vessels precontracted with NE but had no effect on KCl precontracted vessels. However,the relaxation effect of Sal B was not significantly inhibited by NG-nitro-L-arginine methylester（ L-NAME） and Indomethacin（ Indo）. Also,the relaxation effect of Sal B was not significantly inhibited by tetraethylammonium（ TEA）,4-aminopyridine（ 4-AP）and glibenclamide（ Glib）. The relaxation effect of Sal B was also not significantly inhibited by beta-blocker propranolol. But Sal B can inhibit the contraction vessels induced by extracellular calcium and intracellular calcium and its effect on latter is stronger than that on the former. Conclusion： The mechanisms may involve the reduction in Ca2 ＋influx through the receptor-dependent pathway,voltage-dependent pathway and blocking the IP3 receptorinduced Ca2 ＋release,but not correlated with NO-guanylyl cyclase pathway,COX pathway,K＋channels or βreceptor.
出处
《中国实验方剂学杂志》
CAS
CSCD
北大核心
2016年第23期121-126,共6页
Chinese Journal of Experimental Traditional Medical Formulae
基金
国家"重大新药创制"科技重大专项(2011ZX09102-002-07)
