泽泻对肝硬变大鼠主动脉的扩血管作用及机制

Endothelium-dependent Relaxation Effect of Rhizoma Alismatis in Aortic Rings of Liver Cirrhotic Rats

目的 :探讨泽泻的扩血管作用与血管内皮的联系。方法 :取正常和肝硬变大鼠的胸主动脉环进行离体血管张力实验。应用一氧化氮 (NO)合成的前体物质 L -精氨酸 (L - Arg)、NO合成酶抑制剂 NG-硝基 - L -精氨酸甲酯(L - NAME)、前列环素 (PGI2 )拮抗剂吲哚美辛 (Indo)以及机械方法去除血管内皮等干预 ,测定泽泻的扩血管活性。结果 :1泽泻的扩血管作用随其反应浓度的增加而增大。 2应用 Indo和 L - NAME后 ,可使对照组和肝硬变组离体血管的扩张作用明显减弱 (P <0 .0 1) ,但应用 L - Arg后未见扩血管作用的明显增加。3机械去除血管内皮后 ,泽泻的扩血管作用受到明显抑制 [对照组 (2 0 7.5± 4 9.4 ) mg降至 (132 .5± 2 2 .2 ) m g,P <0 .0 1];肝硬变组 [(2 70 .0±77.5 ) mg降至 (10 0 .0± 4 2 .4 ) m g,P <0 .0 1]。结论 :泽泻对肝硬变大鼠主动脉环的扩血管作用机制 ,是部分血管内皮依赖性的 ,可能通过血管内皮细胞增加 PGI2 和 NO的释放而发挥扩血管作用。

Objective:To assess the relationship between the released nitric oxide (NO) prostacyclin (PGI 2) in vascular endothelium and vasodilation effects of Rhizoma Alismatis. Methods: Thoracic aortic rings from normal and liver cirrhotic rats were mounted in tissue bath containing physiologic Kreb's solution. Under resting tension, endothelium dependent relaxative response to Rhizoma Alismatis was studied in the absence or presence of NO synthase inhibitor (L N G nitroarginine methyl ester, L NAME), NO synthase substrate (L arginine, L Arg), cyclooxygenase inhibitors (indomethacin). Blood vessel endothelia were denuded. Results: ①Rhizoma Alismatis could lead to a concentration dependent vasodilatation activity. ②Vasodilation activity of Rhizoma Alismatis was markedly attenuated by pretreatment with indomethacin and L NAME (P< 0.01 ), but not Arginine.③After the removal of the endothelium from the aorta rings, the vasodilation activity of Rhizoma Alismatis was significantly inhibited in control group [(207.5±49.4)mg(132.5±22.2)mg, P<0.01] and liver cirrhosis rats [(270.0±77.5)mg(100.0±42.4)mg, P<0.01]. Conclusion: Rhizoma Alismatis induced relaxation in rat aorta was partially endothelium dependent, which may depend on released PGI 2 and NO in vascular endothelium stimulated by Rhizoma Alismatis.