Nikolaev V P
Department of Extravehicular Activity, Institute of Biomedical Problems, Moscow, Russia.
Aviat Space Environ Med. 2000 Jul;71(7):723-9.
To gain insight into the special nature of gas bubbles that may form in astronauts, aviators and divers, we developed a mathematical model which describes the following: 1) the dynamics of extravascular bubbles formed in intercellular cavities of a hypothetical tissue undergoing decompression; and 2) the dynamics of nitrogen tension in a thin layer of intercellular fluid and in a thick layer of cells surrounding the bubbles. This model is based on the assumption that, due to limited cellular membrane permeability for gas, a value of effective nitrogen diffusivity in the massive layer of cells in the radial direction is essentially lower compared to conventionally accepted values of nitrogen diffusivity in water and body tissues. Due to rather high nitrogen diffusivity in intercellular fluid, a bubble formed just at completion of fast one-stage reduction of ambient pressure almost instantly grows to the size determined by the initial volume of the intercellular cavity, surface tension of the fluid, the initial nitrogen tension in the tissue, and the level of final pressure. The rate of further bubble growth and maximum bubble size depend on comparatively low effective nitrogen diffusivity in the cell layer, the tissue perfusion rate, the initial nitrogen tension in the tissue, and the final ambient pressure. The tissue deformation pressure performs its conservative action on bubble dynamics only in a limited volume of tissue (at a high density of formed bubbles). Our model is completely consistent with the available data concerning the random latency times to the onset of decompression sickness (DCS) symptoms associated with hypobaric decompressions simulating extravehicular activity. We believe that this model could be used as a theoretical basis for development of more adequate methods for the DCS risk prediction.
为深入了解可能在宇航员、飞行员和潜水员体内形成的气泡的特殊性质,我们开发了一个数学模型,该模型描述了以下内容:1)在经历减压的假设组织的细胞间腔中形成的血管外气泡的动力学;2)气泡周围细胞间液薄层和厚细胞层中氮张力的动力学。该模型基于这样的假设,即由于细胞膜对气体的渗透性有限,在径向方向上大量细胞层中有效氮扩散率的值与水中和身体组织中通常接受的氮扩散率值相比显著较低。由于细胞间液中氮扩散率相当高,在环境压力快速单阶段降低刚完成时形成的气泡几乎瞬间就会生长到由细胞间腔的初始体积、液体的表面张力、组织中的初始氮张力和最终压力水平决定的大小。气泡进一步生长的速率和最大气泡大小取决于细胞层中相对较低的有效氮扩散率、组织灌注率、组织中的初始氮张力和最终环境压力。组织变形压力仅在有限的组织体积中(在形成气泡的高密度情况下)对气泡动力学发挥其保守作用。我们的模型与关于模拟舱外活动的低压减压相关的减压病(DCS)症状发作的随机潜伏期的现有数据完全一致。我们认为,该模型可作为开发更合适的DCS风险预测方法的理论基础。