摘要
目的:研究中成药华蟾素对大鼠离体胸主动脉环的作用及其机制。方法:采用大鼠离体胸主动脉灌流模型,观察华蟾素对血管张力的影响。结果:华蟾素(2.5、5.0、7.5、10.0 g/L)浓度依赖性地收缩去内皮的大鼠胸主动脉环,收缩幅度分别为(16.3±3.39)%、(52.5±7.70)%、(60.9±8.84)%、(69.2±11.34)%,显著高于内皮完整的大鼠胸主动脉环收缩幅度[(6.2±2.07)%、(14.7±4.91)%、(17.6±5.86)%、(20.3±6.78)%](P<0.01);在无Ca2+液中,10.0 g/L华蟾素对去内皮主动脉环的收缩幅度[(7.1±0.79)%]显著低于有Ca2+液中的收缩幅度[(78.1±4.32)%](P<0.01);维拉帕米(1-0 7m o l/L,V er)预处理可消除10.0 g/L华蟾素的缩血管作用(P<0.01);一氧化氮合酶抑制剂L-NAM E(1-0 4m o l/L)预处理内皮完整的主动脉环,可增强10.0 g/L华蟾素的缩血管作用(P<0.01)。结论:华蟾素对大鼠离体胸主动脉有收缩作用,其缩血管机制与其促使细胞外Ca2+经电压依赖性钙通道内流进入血管平滑肌细胞有关;同时,华蟾素作用于血管内皮细胞,引起血管舒张因子一氧化氮的释放,部分抵消其缩血管效应。
Objective: To examine the effect of cinobufacini on rat thoracic aorta and its mechanism. Methods: Isolated rat thoracic aorta was perfused and isometric tension was recorded by organ bath technique before and after cinobufacini treatment. Results: Cinobufacini induced contraction of isolated thoracic aorta with or without endothelium in a concentration-dependent manner (at concentration of 2.5, 5.0, 7.5, 10.0 g/L). The vasoconstriction effect of cinobufacini was more potent in endothelium-denuded aorta ring [(16.3±3.39)%, (52.5±7.70)%, (60.9±8.84)%, (69.2±11.34)%] than in endothelium-intact aorta ring [(6.2±2.07)%, (14.7±4.91)%, (17.6±5.86)%, (20.3±6.78)%(P〈0.01)]. Its contractile effect was attenuated in Ca^2+-free solution (about 1/10 of that in buffer with 1.25 mmol/L CaCl2) or by the treatment with verapamil (10^-7 mol/L), an L-type calcium channel antagonist. Cinobufacini induced contraction on the endothelium-intact rat aorta was augmented by pretreatment with L-NAME (10^-4mol/L), a nitric oxide synthase inhibitor. Conclusion: Cinobufacini contracts rat thoracic aorta by opening the voltage-dependent Ca^2+ channel and increasing Ca^2+ influx into vascular smooth muscle. Cinobufacini can also stimulate the release of vascular relaxant factor, nitric oxide, from the endothelium and thus antagonize cinobufacini-induced contraction.
出处
《浙江大学学报(医学版)》
CAS
CSCD
2006年第2期178-181,共4页
Journal of Zhejiang University(Medical Sciences)
基金
浙江省教育厅科研基金项目(20040205)