Sexually dimorphic response of the balloon-injured rat carotid artery to hormone treatment.
Sexually dimorphic response of the balloon-injured rat carotid artery to hormone treatment.
复制标题
气球损伤的大鼠颈动脉对激素治疗的性别二态性反应。
DOI：
10.1161/01.cir.95.5.1301
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发表时间：
1997
期刊：
影响因子：
37.8
通讯作者：
Chen,YF
中科院分区：
文献类型：
--
作者：
Oparil,S;Levine,RL;Chen,SJ;Durand,J;Chen,YF
背景雌激素钝化去性腺大鼠血管损伤后的新生内膜反应；添加孕激素可阻断雌激素的作用。本研究在完整的大鼠上测试了(1)外源性雌激素对损伤的颈动脉是否有血管保护作用，(2)孕激素(甲孕酮，MPA)是否阻断了雌激素的血管保护作用，(3)雌激素和(或)甲孕酮对性二相性反应的影响可以通过血清17β-雌二醇水平的差异来解释。两周后，大鼠被过量的戊巴比妥杀死，颈动脉的肌内膜增厚进行了评估。雌二醇和甲孕酮都不能改变男性的新生内膜反应。雌鼠血清17β-雌二醇水平达到生理水平(雌鼠)，但雌鼠对雌激素的血管保护作用无明显影响，但雌鼠对雌激素的血管保护作用有抑制作用。甲孕酮增强完整女性的新生内膜反应，可能是通过阻断内源性雌激素的产生从而起到血管保护作用。
BackgroundEstrogen blunts the neointimal response to vascular injury in gonadectomized rats of both sexes; addition of a progestin blocks the estrogen effect. This study tested, in intact rats of both sexes, whether (1) exogenous estrogen has a vasoprotective effect in injured carotid arteries, (2) progestin (medroxyprogesterone acetate, MPA) blocks the vasoprotective effect of estrogen, and (3) any observed sexual dimorphism in the responses to estrogen and/or MPA can be accounted for by differences in serum 17β-estradiol levels.Methods and ResultsIntact male and female Sprague-Dawley rats were randomly divided into four subgroups treated with either (1) 17β-estradiol, (2) MPA, (3) 17β-estradiol+MPA, or (4) vehicle and were subjected to balloon injury of the right common carotid artery. Two weeks later, rats were killed by an overdose of pentobarbital, and the carotid arteries were evaluated for myointimal thickening. Neither estradiol nor MPA altered the neointimal response in males. In females, estradiol reduced and MPA enhanced the response, whereas addition of MPA to estradiol blocked the vasoprotective effects of estrogen.ConclusionsIntact male rats but not intact females are resistant to the vasoprotective effects of exogenous estrogen, despite attainment of physiological (for females) serum 17β-estradiol levels. MPA enhances the neointimal response in intact females, presumably by blocking the production and thus the vasoprotective effect of endogenous estrogen.