实验动物脑室大小与毛细血管压力之间关系的数学模型

A. A. Cherevko, G. Valova, D. V. Petrovsky, A. E. Akulov
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引用次数: 0

摘要

目的:调整描述流体介质与脑物质之间相互作用的数学模型,以确定 BALB/c 和 C57BL/6 两种基因型实验动物脑室大小与毛细血管压力之间的关系。材料和方法研究对象为 12 周龄的 C57BL/6 和 BALB/c 近交系雄性小鼠各 4 只。使用 11.7 T 水平 MR 扫描仪(Bruker,BioSpec 117/16 USR,德国)获取大脑和脑脊液系统图像。数学建模选择了距前囟-0.5毫米处的轴向切面。为了描述所获得的数据,数学模型根据人类和小鼠脑脊液形成率的已知值选择了一个比例因子。结果与讨论所有动物的毛细血管压力和平均心室壁位移之间的关系都有相同的定性模式。虽然所选的遗传品系 BALB/c 和 C57Bl 小鼠在脑室大小方面存在显著差异,但这些动物基因型的差异并不影响这种关系的性质。在压缩或中度脑室扩张区域改变流体介质相互作用的参数几乎不会导致脱离生理上可接受的毛细血管压力值。在这种情况下,心室的大小会发生显著变化。相反,在心室大面积扩张的区域,心室大小几乎不会发生变化,但毛细血管压力却会急剧增加,远远超出生理极限。因此,心室大小的变化是一个适应过程,与颅内液体流动变化引起的压力波动有关。在心室大小几乎没有变化的情况下,某些值达到了生理上不可接受的压力范围,事实上这与死亡有关,这一事实表明这种情况很少发生,但在颅内流体介质流动受到破坏,心室大小的增加限制了适应能力的情况下,这种情况是可能发生的。结论。所展示的动物模型将进一步加深对我们所建立的模式的理解,并使我们能够继续尝试进行预测。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mathematical model of the dependence between cerebral ventricular size and capillary pressure in laboratory animals
Aim: To adapt a mathematical model describing the interaction between fluid media and brain matter for the purpose of definition of the dependence between brain ventricle size and capillary pressure in laboratory animals of two genotypes, BALB/c and C57BL/6. Material and methods. The study included 4 male mice of each inbred strain C57BL/6 and BALB/c at the age of 12 weeks. The brain and cerebrospinal fluid system images were obtained using an 11.7 T horizontal MR scanner (Bruker, BioSpec 117/16 USR, Germany). An axial section at the level of -0.5 mm from bregma was chosen as the geometry for mathematical modelling. To describe the data obtained, the mathematical model was adapted by selecting a scale factor based on the known values of the cerebrospinal fluid formation rate for humans and mice. Results and discussion. The same qualitative pattern of relationship between capillary pressure and mean ventricular wall displacement was observed for all animals considered. Although the selected genetic strains of BALB/c and C57Bl mice differ significantly in terms of cerebral ventricle size, these differences in animal genotype did not affect the nature of this relationship. Changing the parameters of the fluid media interaction in the area of compression or moderate ventricular dilation almost does not lead to an exit from the physiologically acceptable capillary pressure value. In this case, the size of the ventricles changes significantly. In the area of large ventricular dilation, in contrast, there is little change in ventricular size, and this is accompanied by a dramatic increase in capillary pressure far beyond physiologic limits. Thus, the change in ventricular size is an adaptive process associated with pressure fluctuations caused by changes in intracranial fluid flow. The mere fact that some of the values reach the zone of physiologically unacceptable pressures associated, in fact, with death, provided that there is practically no change in ventricular size indicates that such a situation is rarely realized and is possible in case of violation of intracranial fluid media flows associated with the fact that the increase in ventricular size limits adaptive capabilities. Conclusions. The presented animal model will further increase the understanding of the pattern we have established and allow us to move on to attempts at prediction.
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