雌激素对兔动脉粥样硬化形成及某些体液因子的影响

The effect of estrogen on atherosclerosis and some vasoactive factors in rabbits

目的 建立雌激素抗兔动脉粥样硬化模型 ,阐明雌激素作用的可能机制。 方法 2 1只纯种新西兰兔随机分入 :A组 (切除卵巢未补充雌激素 )、B组 (切除卵巢补充雌激素 )、C组 (未切除卵巢 ) ,给予 1%胆固醇饮食 ,8周时比较动脉形态学变化 ,测定动脉一氧化氮及一些体液因子。 结果 (1) A组兔主动脉内膜面积〔(1.35± 0 .44 ) m m2 〕高于 B、C组〔(0 .2 0± 0 .2 9)及 (0 .34± 0 .2 9) mm2 〕(P<0 .0 5 ) ;(2 ) A组兔内皮素 - 1高于 B组及 C组 (P<0 .0 5及 P<0 .0 1) ,血浆肾素活性、血管紧张素 高于 C组 (P<0 .0 5 ) ;(3) B、C组血浆雌二醇〔(2 12± 78)及 (2 2 9± 10 3) ng/ L〕和主动脉一氧化氮〔(0 .41± 0 .18)及 (0 .44± 0 .16 ) nmol/ m g〕高于 A组〔(10 3± 6 9) ng/ L及 (0 .2 5± 0 .0 6 ) nm ol/ m g〕(P<0 .0 5 )。 结论 雌激素可明显抑制动脉粥样硬化形成 ,可能与促进一氧化氮生成、抑制内皮素生成、抑制肾素血管紧张素系统活性有关。

Objective To creat an anti atherosclerosis animal model with estrogen and to clarify the possible mechanisms of estrogen against atherosclerosis. Methods Twenty one female New Zeland white rabbits were assigned to 3 groups, group A: oophorectomized , group B: oophorectomized and receiving 17 β estradiol treatment, group C: with sham operation. Each rabbit was given 1% cholesterol diet. Eight weeks later, the aorta was taken for morphological analysis of the intima and nitric oxide production.The plasma endothelin 1, renin activity and angiotensin Ⅱ were also measured. Results (1) The area of the aortic intima in group A〔(1 35±0 44) mm 2〕 was larger than that in group B and group C〔(0 20±0 29,0 34±0 29) mm 2〕.(2)Plasma endothelin 1 was significantly higher in group A than that in group B and group C. Plasma renin activity and angiotensin Ⅱ in group A were higher than those in group C ( P <0 05). (3) The production of NO by aorta exposed to 10 -5 mol/L acetylcholine increased significantly ( P <0 05) in group B and group C〔(0 41±0 18,0 44±0 16) nmol/mg〕,as compared with group A〔(0 25±0 06) nmol/mg〕( P <0 05). It also increased significantly ( P <0 05) in group B and group C as compared with the same group without exposure to acetylcholine; this effect was not observed in group C. Conclusions 17 β estradiol could inhibit the progress of atherosclerosis in the oophorectomized rabbits. It could enhance the production of No and inhibit the production of endothelin 1 and the activity of the renin angiotensin system.These changes may play important roles in the mechanism of estrogen against atherosclerosis.