A study on the biologic control over heart rate changes in the human fetus simulated using a mathematical model.

为了评估人类胎儿心率(FHR)变化的生物控制的发育过程，我们设计了一个适用于FHR和心跳差(BBDS)的数学分析模型。使用计算机系统对FHR矩阵的特殊设计模型进行因子分析。该矩阵分别按行和列以1拍/分钟(BPM)的间隔排列FHR和BBD。在通过从给定的一对连续的两个FHR中的后续FHR减去之前的FHR来获得BBD之后，将之前的FHR和BBD的两个变量交叉，并在矩阵的相应元素处记录数字1。对所有FHR和BBD进行此程序，得到包含累积发病率的矩阵。如BBD集群所示，三个不同的因素变得明显：在零bpm附近波动，加上偏差和负偏差。第一个被认为在维持所谓的基础心率方面起作用，第二个和第三个分别表示对FHR的加速和减速作用。至于基础心率的时间变化，有5个不同的独立因素，它们与胎龄有很好的相关性。在妊娠28-30周、32-33周和35-36周时，几种独立的和潜在的调节基础心率的机制会有所不同，并随着胎龄的增加而发展。虽然无脑胎儿没有这些发现，但脑膨出的胎儿表现出与正常胎儿相似的FHR个体发育。因此，这些FHR变化的调节机制被归因于位于延髓水平或更高水平的功能，至少在人类胎儿近月阶段是这样。在计算机模拟实验中，该分析模型对于FHR-Study的复杂模型是可扩展的。

To evaluate the developmental process with respect to biologic control over heart rate (FHR) changes in the human fetus, we have devised a model suitable for mathematical analysis of both FHRs and beat-to-beat differences (BBDs). Factor analysis was applied, using a computer system, on a specially devised model of an FHR matrix. This matrix was arranged with FHRs and BBDs at 1-beat/minute (bpm) intervals by row and columns, respectively. After obtaining the BBD by subtracting the antecedent FHR from the following FHR in a given pair of two consecutive FHRs, both variables of the antecedent FHR and BBD were crossed and a number 1 was recorded at the corresponding element of the matrix. This procedure was done for all pairs of FHR and BBD yielding a matrix containing the cumulative incidences. As indicated by clusters of BBDs, three different factors become evident: fluctuation around zero bpm, plus deviations and minus deviations. The first was considered to play a role in maintaining so-called basal heart rates, and the second and the third indicate accelerating and decelerating actions on FHRs, respectively. As for chronological changes in basal heart rates, there were noted 5 different and independent factors, which correlated well with gestational age. Several isolated and underlying mechanisms regulating basal heart rates differentiate at definite periods: 28-30, 32-33 and 35-36 weeks of gestation and develop functionally with advancing fetal age. Although these findings were absent in anencephalic fetuses, fetuses with encephalocele showed ontogeny of FHRs similar to those seen in normal fetuses. Therefore, the regulatory mechanisms of these FHR changes were attributed to functions located at the level of the medulla or higher, at least in the human fetus near term. This analytical model was found to be extensible for a complex model of FHR-study in a computer-simulation experiment.