Longo L D
Am J Physiol. 1983 Nov;245(5 Pt 1):R720-9. doi: 10.1152/ajpregu.1983.245.5.R720.
During the course of gestation the increase of maternal total blood volume and cardiac output may result from two mechanisms acting in concert: 1) the production of several hormones by the fetus and the placenta, and 2) the uteroplacental circulation acting as an arteriovenous shunt. Plasma volume appears to increase as a consequence of renal Na+ reabsorption and water retention, which result from increased aldosterone production via the renin-angiotensin system, as a consequence of placental estrogen production. This estrogen production in turn results from increasing availability of the estrogen substrate dehydroepiandrosterone (chiefly from the fetal adrenal gland). Erythrocyte volume increases as a consequence of the erythropoietic effect of placental chorionic somatomammotropin, progesterone, and perhaps prolactin. In addition, maternal blood volume increases in response to the uteroplacental circulation functioning as a low-resistance circuit. In turn, this increases cardiac output and nutrient delivery for further growth of the products of gestation. Thus there may exist a feedback mechanism whereby fetal growth and, in particular, increasing steroidogenesis by the developing fetal adrenal gland result in the maternal cardiovascular adaptations to pregnancy that optimize further fetal development. In certain complications of pregnancy the less-than-normal maternal blood volume increase may result from failure of these mechanisms, while in turn contributing to the further genesis of these disorders.
在妊娠期，母体总血容量和心输出量的增加可能是由两种协同作用的机制导致的：1）胎儿和胎盘产生的几种激素；2）子宫胎盘循环作为动静脉分流。血浆量的增加似乎是由于肾钠重吸收和水潴留，这是由胎盘雌激素生成导致肾素 - 血管紧张素系统中醛固酮生成增加所致。而这种雌激素生成又是由于雌激素底物脱氢表雄酮（主要来自胎儿肾上腺）可用性增加引起的。红细胞量的增加是胎盘绒毛膜生长催乳素、孕酮以及可能还有催乳素的促红细胞生成作用的结果。此外，母体血容量因子宫胎盘循环作为低阻力循环而增加。这进而增加心输出量和营养物质输送，以促进妊娠产物的进一步生长。因此，可能存在一种反馈机制，即胎儿生长，特别是发育中的胎儿肾上腺类固醇生成增加，导致母体心血管系统适应妊娠，从而优化胎儿的进一步发育。在某些妊娠并发症中，母体血容量增加低于正常可能是这些机制失灵的结果，而这反过来又会促使这些疾病进一步发生。
