McCrohon J A, Walters W A, Robinson J T, McCredie R J, Turner L, Adams M R, Handelsman D J, Celermajer D S
Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia.
J Am Coll Cardiol. 1997 Jun;29(7):1432-6. doi: 10.1016/s0735-1097(97)00063-6.
We sought to assess whether high dose estrogen treatment is associated with enhanced arterial reactivity in genetic males.
Although estrogens have been shown to enhance arterial reactivity in women, and are thereby thought to confer cardiovascular benefit, the vascular effects of long-term estrogen therapy in genetic males is unknown.
We studied the arterial physiology of 30 genetic males--15 male to female transsexuals receiving long-term high dose estrogen therapy and 15 healthy male control subjects matched for age, smoking history and vessel size. Using external vascular ultrasound, brachial artery diameter was measured at rest, after flow increase (causing endothelium-dependent dilation [EDD]) and after nitroglycerin (GTN), an endothelium-independent dilator. Blood pressure, cholesterol and testosterone levels were also measured in each subject.
Total testosterone and free testosterone index levels were lower in the transsexuals compared with the control subjects (p < 0.001). In contrast, EDD was significantly higher in the transsexuals than in the control males (mean [+/-SD] 7.1 +/- 3.1% vs. 3.2 +/- 2.8%, p = 0.001), as was the GTN response (21.2 +/- 6.7% vs. 14.6 +/- 3.3%, p = 0.002). Total and high density lipoprotein cholesterol, blood pressure levels and baseline vessel size were similar in the two groups. On multivariate analysis, enhanced EDD was associated independently with estrogen therapy (p = 0.02) and with low total cholesterol (p = 0.04). An enhanced GTN response was also significantly associated with estrogen therapy (p = 0.03).
Long-term treatment with high dose estrogens is associated with enhanced arterial reactivity in genetic males, which may be due to the effects of estrogen excess or androgen deprivation, or both.
我们试图评估高剂量雌激素治疗是否与基因男性的动脉反应性增强有关。
尽管雌激素已被证明可增强女性的动脉反应性，因此被认为具有心血管益处，但长期雌激素治疗对基因男性的血管影响尚不清楚。
我们研究了30名基因男性的动脉生理学——15名接受长期高剂量雌激素治疗的男变女变性者和15名年龄、吸烟史和血管大小相匹配的健康男性对照者。使用外部血管超声，在静息状态下、血流增加后（引起内皮依赖性舒张[EDD]）以及在使用硝酸甘油（GTN，一种非内皮依赖性舒张剂）后测量肱动脉直径。还测量了每位受试者的血压、胆固醇和睾酮水平。
与对照者相比，变性者的总睾酮和游离睾酮指数水平较低（p<0.001）。相比之下，变性者的EDD显著高于对照男性（平均值[±标准差]7.1±3.1%对3.2±2.8%，p = 0.001），GTN反应也是如此（21.2±6.7%对14.6±3.3%，p = 0.002）。两组的总胆固醇和高密度脂蛋白胆固醇、血压水平和基线血管大小相似。多变量分析显示，EDD增强独立与雌激素治疗相关（p = 0.02）以及总胆固醇水平低相关（p = 0.04）。GTN反应增强也与雌激素治疗显著相关（p = 0.03）。
高剂量雌激素长期治疗与基因男性的动脉反应性增强有关，这可能是由于雌激素过多或雄激素缺乏，或两者共同作用的结果。
