Arieli Ran
Israel Naval Medical Institute, Israel Defence ForceHaifa, Israel.
Eliachar Research Laboratory, Western Galilee Medical CenterNahariya, Israel.
Front Physiol. 2017 Aug 15;8:591. doi: 10.3389/fphys.2017.00591. eCollection 2017.
Decompression illness (DCI) occurs following a reduction in ambient pressure. Decompression bubbles can expand and develop only from pre-existing gas micronuclei. The different hypotheses hitherto proposed regarding the nucleation and stabilization of gas micronuclei have never been validated. It is known that nanobubbles form spontaneously when a smooth hydrophobic surface is submerged in water containing dissolved gas. These nanobubbles may be the long sought-after gas micronuclei underlying decompression bubbles and DCI. We exposed hydrophobic and hydrophilic silicon wafers under water to hyperbaric pressure. After decompression, bubbles appeared on the hydrophobic but not the hydrophilic wafers. In a further series of experiments, we placed large ovine blood vessels in a cooled high pressure chamber at 1,000 kPa for about 20 h. Bubbles evolved at definite spots in all the types of blood vessels. These bubble-producing spots stained positive for lipids, and were henceforth termed "active hydrophobic spots" (AHS). The lung surfactant dipalmitoylphosphatidylcholine (DPPC), was found both in the plasma of the sheep and at the AHS. Bubbles detached from the blood vessel in pulsatile flow after reaching a mean diameter of ~1.0 mm. Bubble expansion was bi-phasic-a slow initiation phase which peaked 45 min after decompression, followed by fast diffusion-controlled growth. Many features of decompression from diving correlate with this finding of AHS on the blood vessels. (1) Variability between bubblers and non-bubblers. (2) An age-related effect and adaptation. (3) The increased risk of DCI on a second dive. (4) Symptoms of neurologic decompression sickness. (5) Preconditioning before a dive. (6) A bi-phasic mechanism of bubble expansion. (7) Increased bubble formation with depth. (8) Endothelial injury. (9) The presence of endothelial microparticles. Finally, constant contact between nanobubbles and plasma may result in distortion of proteins and their transformation into autoantigens.
减压病(DCI)发生于环境压力降低之后。减压气泡只能从预先存在的气体微核中膨胀并形成。迄今为止,关于气体微核的成核和稳定提出的不同假说从未得到验证。已知当光滑的疏水表面浸入含有溶解气体的水中时,纳米气泡会自发形成。这些纳米气泡可能是长期以来寻找的减压气泡和减压病背后的气体微核。我们将疏水性和亲水性硅片置于水下并施加高压。减压后,疏水性硅片上出现了气泡,而亲水性硅片上没有。在另一系列实验中,我们将大型羊血管置于冷却的高压舱中,压力为1000 kPa,持续约20小时。在所有类型的血管中,气泡在特定部位形成。这些产生气泡的部位脂质染色呈阳性,因此被称为“活性疏水部位”(AHS)。在绵羊的血浆中和AHS处均发现了肺表面活性物质二棕榈酰磷脂酰胆碱(DPPC)。气泡在达到平均直径约1.0毫米后,在脉动血流中从血管上脱离。气泡膨胀是双相的——一个缓慢的起始阶段,在减压后45分钟达到峰值,随后是快速的扩散控制生长阶段。潜水减压的许多特征与血管上AHS的这一发现相关。(1) 有气泡形成者和无气泡形成者之间的差异。(2) 与年龄相关的影响和适应性。(3) 第二次潜水时减压病风险增加。(4) 神经减压病的症状。()潜水前的预处理。(6) 气泡膨胀的双相机制。(7) 气泡形成随深度增加。(8) 内皮损伤。(9) 内皮微粒的存在。最后,纳米气泡与血浆之间的持续接触可能导致蛋白质变形并转化为自身抗原。