Ford S P
J Anim Sci. 1982;55 Suppl 2:32-42.
Current investigations strongly indicate a relationship between the function of adrenergic (vasoconstrictor) nerves innervating uterine and ovarian arteries and local concentrations of estrogen and progesterone. During the estrous cycle of ewes, cows and sows, the higher the estrogen:progesterone ratio in systemic blood, the greater is the quantity of blood flowing through the uterine vascular bed. When converted to a catechol form, estrogen may reduce uterine vasoconstriction by binding to and suppressing perivascular alpha-adrenergic receptor activity. Progesterone, in contrast to estrogen, augments the responsiveness of vascular smooth muscle to norepinephrine. Lymphatic vessels, which are in close linear apposition to the adventitia of the uterine vasculature may serve to transport steroids to the periarterial nerves. Vasodilation associated with steroid-induced changes in autonomic function appears to be modulated and amplified by estrogen-dependent changes in prostaglandin biosynthesis. During early pregnancy in ewes, cows and sows, vasodilation, mediated by the conceptus, occurs in the luteal and (or) uterine vascular beds on days critical for continuation of pregnancy in each species. In cows and sows, this vasodilatory effect of the conceptus is associated with increased concentrations of estrogens in the uterine lumen, as well as the lymph and blood draining the uterus. After the initial increase in blood flow to the uterus during early pregnancy, changes in the estrogen:progesterone ratio in fetal and maternal fluids appear to be unrelated to changes in uterine blood flow (UBF). This lack of association between the estrogen:progesterone ratio and UBF may result from a progressive reduction in number of adrenergic nerves observed in the uterus throughout pregnancy. If one accepts that the estrogen:progesterone ratio controls UBF through alterations in the function of periarterial adrenergic nerves, the impaired function of the nerves during mid and late gestation may preclude the effects of these steroids.
目前的研究强烈表明，支配子宫和卵巢动脉的肾上腺素能（血管收缩）神经功能与雌激素和孕激素的局部浓度之间存在关联。在母羊、母牛和母猪的发情周期中，全身血液中雌激素与孕激素的比例越高，流经子宫血管床的血流量就越大。当转化为儿茶酚形式时，雌激素可能通过结合并抑制血管周围α-肾上腺素能受体活性来减少子宫血管收缩。与雌激素相反，孕激素会增强血管平滑肌对去甲肾上腺素的反应性。与子宫血管外膜紧密呈线性并列的淋巴管可能有助于将类固醇输送到动脉周围神经。与类固醇诱导的自主神经功能变化相关的血管舒张似乎受到前列腺素生物合成中雌激素依赖性变化的调节和放大。在母羊、母牛和母猪的妊娠早期，在每个物种中对维持妊娠至关重要的日子里，由孕体介导的血管舒张发生在黄体和（或）子宫血管床。在母牛和母猪中，孕体的这种血管舒张作用与子宫腔内雌激素浓度的增加以及从子宫引流的淋巴液和血液中的雌激素浓度增加有关。在妊娠早期子宫血流量最初增加之后，胎儿和母体体液中雌激素与孕激素的比例变化似乎与子宫血流量（UBF）的变化无关。雌激素与孕激素比例和UBF之间缺乏关联可能是由于在整个妊娠期间子宫中观察到的肾上腺素能神经数量逐渐减少所致。如果有人认为雌激素与孕激素的比例通过改变动脉周围肾上腺素能神经的功能来控制UBF，那么妊娠中期和晚期神经功能受损可能会排除这些类固醇的作用。
