Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
PLoS One. 2012;7(12):e52273. doi: 10.1371/journal.pone.0052273. Epub 2012 Dec 20.
In mammalian pregnancy, maternal cardiovascular adaptations must match the requirements of the growing fetus(es), and respond to physiologic and pathologic conditions. Such adaptations are particularly demanding for mammals bearing large-litter pregnancies, with their inherent conflict between the interests of each individual fetus and the welfare of the entire progeny. The mouse is the most common animal model used to study development and genetics, as well as pregnancy-related diseases. Previous studies suggested that in mice, maternal blood flow to the placentas occurs via a single arterial uterine loop generated by arterial-arterial anastomosis of the uterine artery to the uterine branch of the ovarian artery, resulting in counter bi-directional blood flow. However, we provide here experimental evidence that each placenta is actually supplied by two distinct arterial inputs stemming from the uterine artery and from the uterine branch of the ovarian artery, with position-dependent contribution of flow from each source. Moreover, we report significant positional- and inter-fetal dependent alteration of placental perfusion, which were detected by in vivo MRI and fluorescence imaging. Maternal blood flow to the placentas was dependent on litter size and was attenuated for placentas located centrally along the uterine horn. Distinctive apposing, inter-fetal hemodynamic effects of either reduced or elevated maternal blood flow, were measured for placenta of normal fetuses that are positioned adjacent to either pathological, or to hypovascular Akt1-deficient placentas, respectively. The results reported here underscore the critical importance of confounding local and systemic in utero effects on phenotype presentation, in general and in the setting of genetically modified mice. The unique robustness and plasticity of the uterine vasculature architecture, as reported in this study, can explain the ability to accommodate varying litter sizes, sustain large-litter pregnancies and overcome pathologic challenges. Remarkably, the dual arterial supply is evolutionary conserved in mammals bearing a single offspring, including primates.
在哺乳动物妊娠中,母体心血管系统的适应性必须满足不断成长的胎儿的需求,并对生理和病理状况做出反应。对于怀有大胎的哺乳动物来说,这种适应性尤其具有挑战性,因为每个胎儿的利益与整个后代的福利之间存在固有冲突。老鼠是研究发育和遗传学以及与妊娠相关疾病最常用的动物模型。先前的研究表明,在老鼠中,胎盘的母体血液供应是通过子宫动脉的动脉-动脉吻合形成的单一动脉子宫环来实现的,这导致了反向双相血流。然而,我们在这里提供了实验证据,表明每个胎盘实际上由来自子宫动脉和卵巢动脉子宫支的两个不同的动脉输入供应,每个来源的血流贡献取决于位置。此外,我们报告了胎盘灌注的显著位置和胎儿间依赖性改变,这是通过体内 MRI 和荧光成像检测到的。胎盘的母体血流取决于胎仔数量,位于子宫角中央的胎盘血流减少。对于位于正常胎儿附近的胎盘,无论是邻近病理胎盘还是低血管 Akt1 缺陷胎盘,都测量到了母体血流减少或增加的独特胎儿间血流的影响。这里报道的结果强调了混淆局部和全身子宫内效应对表型表现的重要性,无论是在一般情况下还是在基因修饰老鼠的情况下。正如本研究所述,子宫血管结构的独特稳健性和可塑性可以解释其适应不同胎仔数量、维持大胎妊娠和克服病理挑战的能力。值得注意的是,这种双重动脉供应在仅生育一胎的哺乳动物中是保守的,包括灵长类动物。