Department of Biomedical Engineering, Tel Aviv University, Tel Aviv, Israel.
Med Eng Phys. 2012 Apr;34(3):364-9. doi: 10.1016/j.medengphy.2011.07.032. Epub 2011 Aug 25.
Fetal growth restriction (FGR) elicits hemodynamic compensatory mechanisms in the fetal circulation. These mechanisms are complex and their effect on the cerebral oxygen availability is not fully understood. To quantify the contribution of each compensatory mechanism to the fetal cerebral oxygen availability, a mathematical model of the fetal circulation was developed. The model was based on cardiac-output distribution in the fetal circulation. The compensatory mechanisms of FGR were simulated and their effects on cerebral oxygen availability were analyzed. The mathematical analysis included the effects of cerebral vasodilation, placental resistance to blood flow, degree of blood shunting by the ductus venosus and the effect of maternal-originated placental insufficiency. The model indicated a unimodal dependency between placental blood flow and cerebral oxygen availability. Optimal cerebral oxygen availability was achieved when the placental blood flow was mildly reduced compared to the normal flow. This optimal ratio was found to increase as the hypoxic state of FGR worsens. The model indicated that cerebral oxygen availability is increasingly dependent on the cardiac output distribution as the fetus gains weight.
胎儿生长受限（FGR）会在胎儿循环中引起血液动力学代偿机制。这些机制很复杂，它们对脑氧供应的影响尚不完全清楚。为了量化每个代偿机制对胎儿脑氧供应的贡献，开发了一个胎儿循环的数学模型。该模型基于胎儿循环中的心输出量分布。模拟了 FGR 的代偿机制，并分析了它们对脑氧供应的影响。数学分析包括脑血管扩张、胎盘血流阻力、静脉导管血液分流程度以及母体来源胎盘功能不全的影响。该模型表明，胎盘血流与脑氧供应之间存在单峰依赖性。与正常血流相比，当胎盘血流轻度减少时，脑氧供应达到最佳。随着 FGR 缺氧状态的恶化，发现这种最佳比值增加。该模型表明，随着胎儿体重的增加，脑氧供应越来越依赖于心输出量分布。
