羟基红花黄色素A对猪冠状动脉环的舒张作用及机制

Vasodilation and mechanism of action of HSYA on porcine coronary artery

目的：研究羟基红花黄色素A（HSYA）对离体猪冠状动脉血管的舒张作用及其可能作用机制，为红花的生物学活性研究和应用提供参考。方法：以猪冠状动脉血管环为材料，以离体血管功能实验方法检测羟基红花黄色素A对猪冠状动脉血管活性作用。结果：羟基红花黄色素A对静息状态猪冠状动脉血管环无明显舒张作用；HSYA在10^-4.5～10^-2mol／L的浓度范围内对PGFh（10^-6mol／L）预收缩的冠状动脉血管环具有浓度依赖性舒张作用，最大舒张效应为124．22％±6．25％，相应的pD2值为2．91±0．23，HSYA的有效剂量为10^-3mol／L，该剂量能使PGF2α（10^-6mol／L）预收缩的冠状动脉血管环达到65．55％±4．15％的舒张效应；HSYA可使KCl的量效曲线下移，呈浓度依赖性。用一氧化氮合成酶抑制剂L—NNA、鸟苷酸环化酶抑制剂亚甲蓝、β受体阻断剂普萘洛尔、β1受体抑制剂atenolol和B2受体抑制剂ICI 118551预处理后，均可明显减弱HSYA诱导的舒张血管作用；前列腺素合成酶抑制剂吲哚美辛，K＋通道抑制剂TEA预处理后，血管舒张作用不能被阻断。结论：羟基红花黄色素A的舒血管活性作用通过内皮．NO．cGMP途径和β-肾上腺素受体途径，并能够阻断血管平滑肌上的电压依赖性钙通道，但与血管平滑肌舒张因子前列腺素的释放及钾离子（KCa）通道无关。

Objective：Through the study of hydroxysaftlor yellow A on isolated porcine coronary artery vascular vasodilation function and its possible mechanism of action, as the study of biological activity and application of safflower reference. Methods：The materials was porcine coronary arterial rings, in vitro vascular function detection of hydroxysafflor yellow A vasoaetive effects. Results：HSYA did not change the resting tension of porcine coronary arterial ring; but HSYA in 10^-4.5 - 10^2 mol/L concentration range showed concentration-dependent relaxant effects with PGF2α （ 10^-6 mol/L） -pre-contracted coronary arteries,the two values were 124.22%± 6.25% （Emax） and 2.91 ±0.23（ pD2 ）. The effective dose of HSYA is 10^-3 mol/L, The dose can make PGF2α（10^-6 mol/L）-pre-contracted coronary arteries get to 65.55% ±4.15% relaxation effect. HSYA inhibited the KCl-induced contraction and downward shifted concentration-response curve of coronary artery rings. Incubation with L-NNA（ an inhibitor of NOS）, methylene blue（ an inhibitor of cGMP synthesis）, propranolol（ β-adrenoceptor antagonist） , β1 -adrenoceptor antagonist atenolol,as well as β2-adrenoceptor antagonist ICI 118551 significantly attenuated the vaso-relaxation in porcine coronary rings induced by HSYA. However, incubation with indomethacin （ an inhibitor of COX）, tetraethylammonium （ an inhibitor of K ＊ channels） did not affect the vaso-relaxation. Conclusion：The effect of HSYA on vasodilator may relate to activation of β2-adrenoceptors, dependent VDCC, and endothelium-NO-cGMP pathway,but not related to PGI2 pathway and potassium channels.