Clarkson T B, Adams M R, Kaplan J R, Shively C A, Koritnik D R
Arteriosclerosis Research Center, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27103.
Am J Obstet Gynecol. 1989 May;160(5 Pt 2):1280-5. doi: 10.1016/s0002-9378(89)80013-4.
The effects on atherogenesis of stress, pregnancy, and oral contraceptive therapy were studied in a nonhuman primate model. The stress of social subordination was associated with ovarian dysfunction, unfavorable lipoprotein changes, and increased coronary artery atherosclerosis compared with nonstressed (socially dominant) or normal monkeys. Although pregnant animals exhibited lower high-density lipoprotein cholesterol concentrations, they had only one half as much diet-induced coronary artery atherosclerosis as their nonpregnant counterparts. Monkeys treated with an Ovral-like regimen also exhibited adverse lipoprotein changes. Nevertheless, prevalence and extent of coronary artery plaques decreased. We conclude that estrogen is an important factor in the animals' "female protection" against diet-induced atherosclerosis. We also suggest that the lowering of high-density lipoproteins by the progestin component of higher-dose contraceptives is not necessarily atherogenic if a sufficiently potent exogenous estrogen is administered concomitantly.
在非人类灵长类动物模型中研究了应激、妊娠和口服避孕药治疗对动脉粥样硬化形成的影响。与无应激（社会主导）或正常猴子相比，社会从属应激与卵巢功能障碍、不利的脂蛋白变化以及冠状动脉粥样硬化增加有关。虽然怀孕动物的高密度脂蛋白胆固醇浓度较低，但它们饮食诱导的冠状动脉粥样硬化程度只有未怀孕同类动物的一半。接受类似Ovral方案治疗的猴子也出现了不利的脂蛋白变化。然而，冠状动脉斑块的患病率和范围有所下降。我们得出结论，雌激素是动物抵抗饮食诱导的动脉粥样硬化的“女性保护”中的一个重要因素。我们还建议，如果同时给予足够有效的外源性雌激素，高剂量避孕药中的孕激素成分导致的高密度脂蛋白降低不一定具有致动脉粥样硬化作用。
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