Arieli Ran, Marmur Abraham
Israel Naval Medical Institute, Haifa, and Eliachar Research Laboratory, Western Galilee Medical Center, Nahariya, Israel
Department of Chemical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.
Physiol Rep. 2017 Mar;5(6). doi: 10.14814/phy2.13191.
Vascular bubble models, which present a realistic biophysical approach, hold great promise for devising suitable diver decompression procedures. Nanobubbles were found to nucleate on a flat hydrophobic surface, expanding to form bubbles after decompression. Such active hydrophobic spots (AHS) were formed from lung surfactants on the luminal aspect of ovine blood vessels. Many of the phenomena observed in these bubbling vessels correlated with those known to occur in diving. On the basis of our previous studies, which proposed a new model for the formation of arterial bubbles, we now suggest the biophysical model presented herein. There are two phases of bubble expansion after decompression. The first is an extended initiation phase, during which nanobubbles are transformed into gas micronuclei and begin to expand. The second, shorter phase is one of simple diffusion-driven growth, the inert gas tension in the blood remaining almost constant during bubble expansion. Detachment of the bubble occurs when its buoyancy exceeds the intermembrane force. Three mechanisms underlying the appearance of arterial bubbles should be considered: patent foramen ovale, intrapulmonary arteriovenous anastomoses, and the evolution of bubbles in the distal arteries with preference for the spinal cord. Other parameters that may be quantified include age, acclimation, distribution of bubble volume, AHS, individual sensitivity, and frequency of bubble formation. We believe that the vascular bubble model we propose adheres more closely to proven physiological processes. Its predictability may therefore be higher than other models, with appropriate adjustments for decompression illness (DCI) data.
血管气泡模型提供了一种现实的生物物理方法，在设计合适的潜水员减压程序方面具有很大的前景。人们发现纳米气泡在平坦的疏水表面上形核，减压后膨胀形成气泡。这种活性疏水斑点（AHS）由绵羊血管腔内的肺表面活性剂形成。在这些冒泡血管中观察到的许多现象与潜水时已知发生的现象相关。基于我们之前提出动脉气泡形成新模型的研究，我们现在提出本文所述的生物物理模型。减压后气泡膨胀有两个阶段。第一个是延长的起始阶段，在此期间纳米气泡转变为气体微核并开始膨胀。第二个较短的阶段是简单的扩散驱动生长阶段，气泡膨胀期间血液中的惰性气体张力几乎保持不变。当气泡的浮力超过膜间力时，气泡就会脱离。应考虑动脉气泡出现的三种潜在机制：卵圆孔未闭、肺内动静脉吻合以及远端动脉中气泡的演变，其中脊髓部位更为常见。其他可以量化的参数包括年龄、适应性、气泡体积分布、AHS、个体敏感性和气泡形成频率。我们认为我们提出的血管气泡模型更紧密地遵循已证实的生理过程。因此，在对减压病（DCI）数据进行适当调整后，其可预测性可能高于其他模型。
