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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.

为了评估生物控制人类胎儿心率（FHR）变化的发育过程，我们设计了一个适合于FHR和搏动差异（BBDs）数学分析的模型。因子分析应用，利用计算机系统，对一个特别设计的模型的FHR矩阵。该矩阵分别以1拍/分钟（bpm）的间隔以行和列排列fhr和bbd。在给定的一对连续的两个FHR中，将前一个FHR减去后一个FHR得到BBD，将前一个FHR和BBD的两个变量进行交叉，并在矩阵的对应元素处记录数字1。对所有对FHR和BBD都进行了该程序，得到一个包含累积发生率的矩阵。正如bbd集群所表明的那样，三个不同的因素变得明显：零bpm附近的波动，加上偏差和减去偏差。第一个被认为在维持所谓的基础心率方面发挥作用，第二个和第三个分别表明加速和减速fhr的作用。在基础心率的时间变化方面，有5个不同且独立的因素与胎龄相关。几个孤立的和潜在的调节基础心率的机制在特定时期（妊娠28- 30,32 -33和35-36周）发生分化，并随着胎龄的增加而功能发展。虽然这些发现在无脑胎儿中不存在，但脑膨出胎儿显示出与正常胎儿相似的fhr个体发育。因此，这些FHR变化的调节机制归因于位于髓质或更高水平的功能，至少在人类胎儿中是这样。在计算机模拟实验中，发现该解析模型可扩展到fhr研究的复杂模型。