Kuhl H
Universitäts-Frauenklinik Frankfurt/M.
Zentralbl Gynakol. 1999;121(2):67-78.
The available epidemiologic data indicate that the sequential addition of progestogens enhances the protective effect of estrogens on the cardiovascular risk. A considerable decrease in LDL-cholesterol is also observed during use of progestogens with androgenic properties. The estrogen-dependent reduction of LDL oxidation is not impaired by progestogens. While estrogens inhibit the endothelial synthesis of adhesion molecules, the activation of monocytes and platelets and the proliferation and migration of smooth muscle cells, the effect of progestogens is rarely investigated. A vasoconstrictory effect of progestogens which may attenuate the estrogen-induced dilation of arteries, was not observed in all clinical investigations. It is presumably based on a reduction of estrogen-stimulated release of nitric oxide by progestogens. In most animal experiments, a progestogen-induced enhancement of contractility of arteries was measured, too. A relaxing effect of progesterone was found in in vitro-experiments, while the results on endothelium-independent effects of synthetic progestogens were contradictory. The sex steroids influence the structure of the vessel wall, whereby the elasticity of arteries is enhanced by estrogens and reduced by progestogens. Oral contraceptives may increase the distensibility of veins which correlates with the hormonal potency of the progestogen. During hormone replacement therapy, venous distensibility is also increased which is mainly due to the action of the estrogen. In vitro experiments with veins revealed a dilatory effect of progestogens. With regard to possible unfavourable effects of progestogens on the vessel wall it is recommended to use the additional progestogen at the minimal effective dose necessary for prevention of endometrial hyperplasia.
现有流行病学数据表明，序贯添加孕激素可增强雌激素对心血管风险的保护作用。在使用具有雄激素特性的孕激素期间，低密度脂蛋白胆固醇也会显著降低。孕激素不会削弱雌激素依赖性的低密度脂蛋白氧化减少作用。虽然雌激素可抑制内皮细胞黏附分子的合成、单核细胞和血小板的活化以及平滑肌细胞的增殖和迁移，但孕激素的作用很少被研究。并非所有临床研究都观察到孕激素可能减弱雌激素诱导的动脉扩张的血管收缩作用。这可能是由于孕激素减少了雌激素刺激的一氧化氮释放。在大多数动物实验中，也测量到了孕激素诱导的动脉收缩性增强。在体外实验中发现孕酮具有舒张作用，而关于合成孕激素非内皮依赖性作用的结果则相互矛盾。性类固醇会影响血管壁结构，其中雌激素可增强动脉弹性，而孕激素则会降低动脉弹性。口服避孕药可能会增加静脉的扩张性，这与孕激素的激素效力相关。在激素替代疗法期间，静脉扩张性也会增加，这主要是由于雌激素的作用。对静脉进行的体外实验显示孕激素具有舒张作用。关于孕激素对血管壁可能产生的不利影响，建议使用预防子宫内膜增生所需的最低有效剂量的附加孕激素。
