Doolette David J
Corresponding author: Associate Professor, Department of Anaesthesiology, The University of Auckland, Auckland, New Zealand,
Diving Hyperb Med. 2019 Mar 31;49(1):64. doi: 10.28920/dhm49.1.64.
Gas micronuclei are gas-filled voids in liquids from which bubbles can form at low gas supersaturation. If water is depleted of gas micronuclei, high gas supersaturation is required for bubble formation. This high gas supersaturation is required in part to overcome the Laplace pressure at the point of transition from dissolved gas to a bubble of perhaps nanometer-scale radius. The sum of gas and vapour partial pressures inside a spherical bubble (Pbub) of radius r exceeds the ambient barometric pressure (Pamb) and is given by the Young-LaPlace equation: Pbub = Pamb + 2γ/r for a bubble not in contact with a solid surface. The second term on the right-hand side is the Laplace pressure across the gas-liquid interface due to surface tension (γ). For instance, for a surface tension characteristic of blood of 0.056 N·m⁻¹, de novo formation of a bubble of r = 10 nm requires gas supersaturation exceeding 2γ/r = 11.2 MPa. However, in humans, detectable venous gas bubbles follow decompression to sea level from as shallow as 138 kPa air saturation, implying gas supersaturation of only a few kPa are required for decompression bubble formation. It is widely accepted that bubbles that form at such low gas supersaturation grow from pre-existing, micron-scale gas micronuclei. For such gas micronuclei to already exist prior to gas supersaturation they cannot simply be small bubbles because positive feedback of Laplace pressure causes a micron radius bubble to dissolve in a fraction of a second. Theoretical candidates for gas micronuclei are bubbles coated in surfactants that counteract the Laplace pressure or crevices where gas voids assume shapes that negate the Laplace pressure. However, to date, the nature of gas micronuclei that underly decompression-induced bubbles and decompression sickness have yet to be identified. Consequently, I was intrigued that in two previous issues of Diving and Hyperbaric Medicine (2018 Volume 48, Issue 2, page 114 and Issue 3, page 197), letters from Ran Arieli to the Editor hypothesized a mechanism for decompression bubble formation in blood vessels and in the skin. Both letters stated "It is known that nanobubbles form spontaneously when a smooth hydrophobic surface is submerged in water containing dissolved gas. We have shown that nanobubbles are the gas micronuclei underlying decompression bubbles and decompression sickness". Surface nanobubbles have been extensively described in the physical chemistry literature, but the second sentence is supported by citation of an hypothesis article. The latter is based on experimental work (referenced therein) in which sections of large blood vessels from sheep were incubated in saline and compressed to 1.013 MPa for 18 hours then rapidly decompressed to the surface, whereupon macroscopic bubbles were photographed forming on the luminal surface of the vessels. The authors speculate that the bubbles were forming from surface nanobubbles on the vessel lumen, but no experimental or analytical evidence was presented that surface nanobubbles were present on the vessel lumen or were the precursors of the observed macroscopic bubbles. Surface nanobubbles form on atomically smooth, hard surfaces in gas supersaturated liquids and, imaged with atomic force microscopy, appear as spherical caps of gas. As far as I can determine, surface nanobubbles have not been reported on biological tissue surfaces. Surface nanobubbles typically have diameters less than 100 nanometers but have lifetimes that are orders of magnitude longer than would a bubble of similar dimensions. Surface nanobubbles do not grow into macroscopic bubbles when exposed to pressure waves sufficient to cause bubble formation from adventitious gas micronuclei elsewhere in the apparatus. This is surely not the last word in this new and active field of research into nanoscopic gas species; however, based on current evidence one must treat with skepticism speculation that unobserved surface nanobubbles are the gas micronuclei from which bubbles form in humans with low gas supersaturation and which underlie decompression sickness.
气体微核是液体中充满气体的空隙,在低气体过饱和度下可从中形成气泡。如果水中缺乏气体微核,则需要高气体过饱和度才能形成气泡。这种高气体过饱和度部分是为了克服从溶解气体转变为可能具有纳米级半径的气泡时的拉普拉斯压力。半径为r的球形气泡(Pbub)内气体和蒸汽的分压之和超过环境气压(Pamb),对于不与固体表面接触的气泡,由杨 - 拉普拉斯方程给出:Pbub = Pamb + 2γ/r。右侧第二项是由于表面张力(γ)在气液界面上的拉普拉斯压力。例如,对于血液特征表面张力为0.056 N·m⁻¹,半径r = 10 nm的气泡的重新形成需要气体过饱和度超过2γ/r = 11.2 MPa。然而,在人类中,从低至138 kPa空气饱和度减压到海平面后可检测到静脉气体气泡,这意味着减压气泡形成仅需要几kPa的气体过饱和度。人们普遍认为,在如此低的气体过饱和度下形成的气泡是从预先存在的微米级气体微核生长而来的。对于在气体过饱和之前就已经存在的这种气体微核,它们不能仅仅是小气泡,因为拉普拉斯压力的正反馈会导致微米半径的气泡在几分之一秒内溶解。气体微核的理论候选者是涂有表面活性剂以抵消拉普拉斯压力的气泡,或者是气体空隙呈现出抵消拉普拉斯压力形状的裂缝。然而,迄今为止,尚未确定导致减压诱导气泡和减压病的气体微核的性质。因此,我对《潜水与高压医学》前两期(2018年第48卷,第2期,第114页和第3期,第197页)中Ran Arieli给编辑的信中提出的血管和皮肤中减压气泡形成机制很感兴趣。两封信都指出:“众所周知,当光滑的疏水表面浸入含有溶解气体的水中时会自发形成纳米气泡。我们已经表明,纳米气泡是减压气泡和减压病的基础气体微核”。表面纳米气泡在物理化学文献中已有广泛描述,但第二句话得到了一篇假设文章的引用支持。后者基于实验工作(其中引用),将绵羊的大血管段在盐水中孵育并压缩至1.013 MPa 18小时,然后迅速减压到表面,随后拍摄到在血管腔表面形成的宏观气泡。作者推测气泡是从血管腔内的表面纳米气泡形成的,但没有提供实验或分析证据表明血管腔内存在表面纳米气泡或它们是观察到的宏观气泡的前体。表面纳米气泡在气体过饱和液体中的原子光滑、坚硬表面上形成,用原子力显微镜成像时,呈现为气体的球形帽。据我所知,尚未有关于生物组织表面存在表面纳米气泡的报道。表面纳米气泡通常直径小于100纳米,但寿命比类似尺寸的气泡长几个数量级。当暴露于足以在设备其他地方由偶然的气体微核引起气泡形成的压力波时,表面纳米气泡不会长大成宏观气泡。在这个关于纳米级气体物种的新的活跃研究领域中,这肯定不是最终定论;然而,基于目前的证据,人们必须对未观察到的表面纳米气泡是人类低气体过饱和度下气泡形成的气体微核以及是减压病基础的推测持怀疑态度。