Hydrodynamics and Interfacial Surfactant Transport in Vascular Gas Embolism

Vascular gas embolism - bubble entry into the blood circulation - is pervasive in medicine, including over 340,000 cardiac surgery patients in the US annually. The gas-liquid interface interacts directly with constituents in blood, including cells and proteins, and with the endothelial cells lining blood vessels to provoke a variety of undesired biological reactions. Surfactant therapy, a potential preventative approach, is based in fluid dynamics and transport mechanics. Herein we review literature relevant to understanding of the key gas-liquid interface interactions inciting injury at the molecular, organelle, cellular and tissue levels, including clot formation, cellular activation, and adhesion events. We review the fluid physics and transport dynamics of surfactant-based interventions to reduce tissue injury from gas embolism. In particular, we focus on experimental research and computational and numerical approaches which demonstrate how surface-active chemical based intervention, based on competition with blood-borne or cell surface-borne macromolecules for surface occupancy of gas-liquid interfaces, alters cellular mechanics, mechanosensing and signaling coupled to fluid stress exposures occurring in gas embolism. We include a new analytical approach for which an asymptotic solution to the Navier-Stokes equations coupled to the convection-diffusion interaction for a soluble surfactant provides additional insight regarding surfactant transport with a bubble in a non-Newtonian fluid.

Tuneable interfacial surfactant aggregates mimic lyotropic phases and facilitate large scale nanopatterning

Self-assembly of insoluble surfactants imposes curvature restrictions on the air–water interface which leads to 3D nanopatterns that can be deposited onto solid surfaces.

Reflectometry Reveals Accumulation of Surfactant Impurities at Bare Oil/Water Interfaces

Bare interfaces between water and hydrophobic media like air or oil are of fundamental scientific interest and of great relevance for numerous applications. A number of observations involving water/hydrophobic interfaces have, however, eluded a consensus mechanistic interpretation so far. Recent theoretical studies ascribe these phenomena to an interfacial accumulation of charged surfactant impurities in water. In the present work, we show that identifying surfactant accumulation with X-ray reflectometry (XRR) or neutron reflectometry (NR) is challenging under conventional contrast configurations because interfacial surfactant layers are then hardly visible. On the other hand, both XRR and NR become more sensitive to surfactant accumulation when a suitable scattering length contrast is generated by using fluorinated oil. With this approach, significant interfacial accumulation of surfactant impurities at the bare oil/water interface is observed in experiments involving standard cleaning procedures. These results suggest that surfactant impurities may be a limiting factor for the investigation of fundamental phenomena involving water/hydrophobic interfaces.

Marangoni-enhanced capillary wetting in surfactant-driven superspreading

Superspreading is a phenomenon such that a drop of a certain class of surfactant on a substrate can spread with a radius that grows linearly with time much faster than the usual capillary wetting. Its origin, in spite of many efforts, is still not fully understood. Previous modelling and simulation studies (Karapetsas et al. J. Fluid Mech., vol. 670, 2011, pp. 5–37; Theodorakis et al. Langmuir, vol. 31, 2015, pp. 2304–2309) suggest that the transfer of the interfacial surfactant molecules onto the substrate in the vicinity of the contact line plays a crucial role in superspreading. Here, we construct a detailed theory to elaborate on this idea, showing that a rational account for superspreading can be made using a purely hydrodynamic approach without involving a specific surfactant structure or sorption kinetics. Using this theory it can be shown analytically, for both insoluble and soluble surfactants, that the curious linear spreading law can be derived from a new dynamic contact line structure due to a tiny surfactant leakage from the air–liquid interface to the substrate. Such a leak not only establishes a concentrated Marangoni shearing toward the contact line at a rate much faster than the usual viscous stress singularity, but also results in a microscopic surfactant-devoid zone in the vicinity of the contact line. The strong Marangoni shearing then turns into a local capillary force in the zone, making the contact line in effect advance in a surfactant-free manner. This local Marangoni-driven capillary wetting in turn renders a constant wetting speed governed by the de Gennes–Cox–Voinov law and hence the linear spreading law. We also determine the range of surfactant concentration within which superspreading can be sustained by local surfactant leakage without being mitigated by the contact line sweeping, explaining why only limited classes of surfactants can serve as superspreaders. We further show that spreading of surfactant spreaders can exhibit either the $1/6$ or $1/2$ power law, depending on the ability of interfacial surfactant to transfer/leak to the bulk/substrate. All these findings can account for a variety of results seen in experiments (Rafai et al. Langmuir, vol. 18, 2002, pp. 10486–10488; Nikolov & Wasan, Adv. Colloid Interface Sci., vol. 222, 2015, pp. 517–529) and simulations (Karapetsas et al. 2011). Analogy to thermocapillary spreading is also made, reverberating the ubiquitous role of the Marangoni effect in enhancing dynamic wetting driven by non-uniform surface tension.

A Computational Approach to Study Heat Transfer Enhancement in Film Boiling due to the Addition of Surfactants

Two-phase flows involving phase change are ubiquitous in a diverse range of scientific and technological applications. There has been great recent interest in the enhancement of boiling heat transfer processes by means of additives such as surfactants. Surfactants can influence boiling through convection currents in the bulk fluids as a result of changes in the surface tension caused by local surfactant concentration due their adsorption/desorption from the bulk regions. This can result in changes in bubble release patterns and higher heat transfer rates if such changes lead to higher rate of vapor formation. We intend to study this effect in the context of film boiling. Our computational approach augments the CLSVOF method with bulk energy and diffusion equations along with a phase change model and an interface surfactant model. The challenge here is to accurately calculate the tangential gradients of the interfacial surfactant concentration in the presence of discontinuous bulk concentration gradients near the interface. We discuss a simplified model in which the interfacial surfactant concentration is always in equilibrium with the changing bulk concentrations and then present validation results to assess the accuracy of this approach. Finally, initial studies of surfactant enhanced film boiling will be presented and interpreted.

Surface tension in situ in flooded alveolus unaltered by albumin

In the acute respiratory distress syndrome, plasma proteins in alveolar edema liquid are thought to inactivate lung surfactant and raise surface tension, T. However, plasma protein-surfactant interaction has been assessed only in vitro, during unphysiologically large surface area compression (%Δ A). Here, we investigate whether plasma proteins raise T in situ in the isolated rat lung under physiologic conditions. We flood alveoli with liquid that omits/includes plasma proteins. We ventilate the lung between transpulmonary pressures of 5 and 15 cmH2O to apply a near-maximal physiologic %Δ A, comparable to that of severe mechanical ventilation, or between 1 and 30 cmH2O, to apply a supraphysiologic %Δ A. We pause ventilation for 20 min and determine T at the meniscus that is present at the flooded alveolar mouth. We determine alveolar air pressure at the trachea, alveolar liquid phase pressure by servo-nulling pressure measurement, and meniscus radius by confocal microscopy, and we calculate T according to the Laplace relation. Over 60 ventilation cycles, application of maximal physiologic %Δ A to alveoli flooded with 4.6% albumin solution does not alter T; supraphysiologic %Δ A raise T, transiently, by 51 ± 4%. In separate experiments, we find that addition of exogenous surfactant to the alveolar liquid can, with two cycles of maximal physiologic %Δ A, reduce T by 29 ± 11% despite the presence of albumin. We interpret that supraphysiologic %Δ A likely collapses the interfacial surfactant monolayer, allowing albumin to raise T. With maximal physiologic %Δ A, the monolayer likely remains intact such that albumin, blocked from the interface, cannot interfere with native or exogenous surfactant activity.