雌激素替代治疗对绝经后妇女血管内皮舒张功能的影响

为了探讨雌激素抗动脉粥样硬化和降低冠心病发病危险的机制 ,采用无创性高分辨超声法观察雌激素替代治疗对绝经后妇女血管内皮依赖性舒张功能的影响 ,于治疗前后测量血清雌二醇、一氧化氮和血脂水平。结果发现 ,绝经后妇女较绝经前妇女血清雌二醇和一氧化氮下降 (P <0 .0 0 1) ,肱动脉血流介导的舒张反应较绝经前明显下降 (3.84 %± 2 .18%比 10 .0 5 %± 3.18% ,P <0 .0 0 1) ;短期雌激素替代治疗后雌二醇和一氧化氮水平较治疗前极显著升高 (P <0 .0 0 1) ,肱动脉血流介导的舒张反应也显著改善 (9.16 %± 3.0 2 % ,P <0 .0 0 1) ,而雌激素替代治疗并未使血脂发生明显改善 (P >0 .0 5 )。相关分析发现肱动脉血流介导的舒张反应与雌二醇和一氧化氮呈正相关(r值分别为 0 .5 6 4和 0 .72 9,P <0 .0 0 1) ,与总胆固醇呈负相关 (r为 - 0 .36 9,P <0 .0 5 )。结果提示短期雌激素替代治疗可明显改善绝经后妇女内皮依赖性舒血管功能障碍 ,且与血脂的改善无关 ,可能与雌激素的直接血管保护作用有关。

Effects of Estrogen Replacement Therapy on Endothelium Dependent Vasodilatory Function in Postmenopausal Women

Aim In order to study effects of estrogen on endothelium dependent vasodilatory function. Methods 32 healthy postmenopausal women regarded as estrogen replacement therapy (ERT) group were treated with conjugated equine estrogen 0.625 mg per day for two weeks, and 24 healthy premenopausal women were regarded as control group. Flow mediated vasodilatory response(FMD) of the brachial artery in ERT and control group were measured by use of high resolution ultrasonography method. Plasma lipids, nitric oxide(NO) and estradiol(E₂) level were also measured. Results Compared with premenopause, plasma E₂ and NO level were significantly decreased(p<0.001), and FMD of the brachial artery also were significantly reduced in postmenopausal women (FMD: 10.05%±3.18% vs. 3.84%±2.18%, p<0.001). After short term ERT, plasma E₂ and NO level were significantly increased(p<0.001), and FMD of the brachial artery also were significantly improved in postmenopausal women (FMD: 9.16%±3.02%, p<0.001), while plasma lipids had no significantly changes before and after ERT. Multiple linear stepwise regression analysis showed that FMD of brachial artery was positively related to NO and E₂(r: 0.729, 0.564, respectively, p<0.001), and was negative related to TC level (r:-0.369, p<0.05). Conclusions Short term ERT can reverse endothelium dependent vasodilatory dysfunction in postmenopausal women. This improvement is not dependent on plasma lipids level, but may be related to the direct vascular protective effects of estrogen, which may be involved in the anti atherogenic action of estrogen.