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

使用数学模型模拟人类胎儿心率变化的生物控制研究。

基本信息

批准号：
60570782
负责人：
KOYANAGI Takashi
金额：
$ 0.96万
依托单位：
Kyushu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1985
资助国家：
日本
起止时间：
1985 至 1987
项目状态：
已结题

项目摘要

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.

为了评估人类胎儿对心率（FHR）变化的生物学控制的发育过程，我们设计了一个适用于FHR和Beat-to-Beat差异（BBD）的数学分析的模型。使用计算机系统在FHR矩阵的特殊设计模型上应用因子分析。该矩阵分别以行/分钟（bpm）间隔分别以行和列的间隔和BBD进行排列。通过在给定两个连续的FHR中从以下FHR中减去前FHR的FHR获得BBD后，越过了前FHR和BBD的两个变量，并在矩阵的相应元素处记录了数字1。对于所有成对的FHR和BBD，完成了包含累积发生率的基质的过程。如BBD的群集所示，三个不同的因素变得明显：BPM零周围的波动，以及偏差和减去偏差。第一个被认为在维持所谓的基础心率方面发挥作用，第二和第三个分别表明对FHR的行动加速和减速。至于基础心率的时间顺序变化，有5个不同且独立的因素，与胎龄相关。几种调节基础心率的分离和潜在的机制在确定的时期有分化：妊娠28-30、32-33和35-36周，并随着胎儿年龄的增长而在功能上发展。尽管这些发现在脑脑胎儿中没有，但脑脑的胎儿表现出类似于正常胎儿中发现的FHR的个体发育。因此，这些FHR变化的调节机制归因于位于髓质或更高水平的功能，至少在人类胎儿近期。在计算机模拟实验中，发现该分析模型对于FHR研究的复杂模型是可扩展的。