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目的研究金丝桃苷对离体大鼠腹主动脉环的舒张作用并探讨其可能的作用机制。方法在大鼠离体腹主动脉环上,分别观察累积浓度的金丝桃苷(1×10-6.5~1×10-4mol/L)对KCl(30mmol/L)和U46619(血栓素类似物,1×10-7mol/L)预收缩血管环的作用。结果金丝桃苷能够浓度依赖性舒张由KC1和U46619预收缩的血管环,最大舒张率分别为(52.2±7.2)%、(80.7±4.1)%;去除血管内皮后,最大舒张率分别降为(15.4±1.2)%、(21.6±1.2)%,与内皮完整组比较有显著差异(P<0.01)。在30mmol/L KCl和1×10-7mol/L U46619预收缩的内皮完整血管环,用一氧化氮(NO)合酶抑制剂(L-NAME,3×10-4mol/L)预温育后,金丝桃苷的最大舒张率分别降为(23.0±3.0)%、(40.3±3.6)%,与未加L-NAME组比较有显著差异(P<0.01);用环氧酶抑制剂吲哚美辛(1×10-5mol/L)预温育对金丝桃苷的舒张血管作用没有明显的影响;在U46619预收缩的血管环,合用L-NAME和吲哚美辛不能完全阻断金丝桃苷引起的血管舒张,最大舒张率为(36.6±1.9)%,与去内皮组比较差异显著(P<0.01)。结论金丝桃苷具有内皮依赖性和较弱的非内皮依赖性血管舒张作用,其内皮依赖性血管舒张可能涉及到内皮NO和内皮依赖性超极化因子(endothelium-derived hyperpolarizing factor,EDHF)的释放。
Objective To study the relaxation effect of hyperoside on the abdominal aorta rings of isolated rat and its possible mechanism. Methods Hyperlipidemia was induced in rats by isolated hyperbranched aortic rings, with cumulative concentrations of hyperoside (1 × 10-6.5 ~ 1 × 10-4 mol / L), KCl (30 mmol / L) and U46619 (thromboxane analogs , 1 × 10-7mol / L) precontracted vascular ring role. Results Hyperin could relax the vascular rings preconstricted by KC1 and U46619 in a concentration-dependent manner. The maximal relaxation rates were (52.2 ± 7.2)% and (80.7 ± 4.1)%, respectively. After removing the vascular endothelium, the maximal diastolic rates were reduced to (15.4 ± 1.2)% and (21.6 ± 1.2)% respectively, which was significantly different from that of the endothelium-intact group (P <0.01). Endothelium intact vessels preconstricted with 30 mmol / L KCl and 1 × 10-7 mol / L U46619 were pre-incubated with nitric oxide synthase inhibitor (L-NAME, 3 × 10-4 mol / L) (23.0 ± 3.0)%, (40.3 ± 3.6)%, respectively, which were significantly different from that of the L-NAME group (P <0.01) Pretreatment with PDMS (1 × 10-5mol / L) had no significant effect on the vasodilator effect of hyperoside; in U46619 precontracted vascular rings, the combination of L-NAME and indomethacin did not completely block Hyperinsuline induced vasodilation, the maximum relaxation rate was (36.6 ± 1.9)%, compared with the endothelium group was significantly different (P <0.01). Conclusions Hyperin has an endothelium-dependent and weaker non-endothelium-dependent vasodilation. Endothelium-dependent vasorelaxation may involve endothelial NO and endothelium-derived hyperpolarizing factor (EDHF) freed.