In this paper the weakly nonlinear stability of two-phase core-annular film flows in the limit of small film thickness and in the presence of both viscosity stratification and interfacial tension is examined. Rational asymptotic expansions are used to derive some novel nonlinear evolution equations for the interface between the phases. The novel feature of the equations is that they include a coupling between core and film dynamics thus enabling a study of its effect on the nonlinear evolution of the interface. The nonlinear interfacial evolution is governed by modified Kuramoto–Sivashinsky equations in the cases of slow and moderate flow [the former also developed by Frenkel, Sixth Symposium on Energy Engineering Sciences (Argonne Lab. Pub. CONF-8805106, 1988), p.100, using different asymptotic methods], which include new nonlocal terms that reflect core dynamics. These equations are solved numerically for given initial conditions and a range of parameters. Some interesting behavior results, such as transition (in parameter space) of chaotic solutions into traveling-wave pulses with more than one characteristic length scale.

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We advance a new hypothesis to explain the changes in hydraulic conductivity of an intact artery wall with transmural pressure previously observed by Tedgui and Lever [Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H784-H791, 1984] and Baldwin and Wilson [Am. J. Physiol. 264 (Heart Circ. Physiol. 33): H26-H32, 1993]. This hypothesis suggests that compaction due to pressure loading of the proteoglycan matrix in the arterial intima near fenestral pores of the internal elastic lamina (IEL) leads to a narrowing of the pore entrance area and a large decrease in local intrinsic Darcy permeability of the matrix. To quantitatively assess the feasibility of this mechanism, a local two-dimensional model is proposed to study filtration flow in the vicinity of fenestral pores in a compressible intima. Using a heterogenous fiber matrix theory, we first predict the change in Darcy permeability with intimal thickness (Li). The model then calculates local velocity profiles and pressure distributions in the intima and media. The results show a marked nonlinear steepening of intimal pressure profiles near fenestral pores when the intima thins at higher luminal pressures. The predicted relative change in resistances of the IEL (with intima, R(I)) and of the media (Rm) shows a steep increase in R(I)/Rm when Li is <20% of its unstressed value. Numerical results also suggest that intimal compression has a limiting behavior in which the much stiffer collagen fibrils inhibit further compaction at high pressures after the proteoglycan matrix is maximally compressed. Predictions are also presented to show how different transmural pressures alter growth of an intimal horseradish peroxidase spot that derives from a localized (a single cell's boundary) endothelial leakage. Such a prediction is amenable to experimental verification.

Compound threads and jets consist of a core liquid surrounded by an annulus of a second immiscible liquid. Capillary forces derived from axisymmetric disturbances in the circumferential curvatures of the two interfaces destabilize cylindrical base states of compound threads and jets (with inner and outer radii R1 and aR1 respectively). The capillary instability causes breakup into drops; the presence of the annular phase allows both the annular- and core-phase properties to influence the drop size. Of technological interest is breakup where the core snaps first, and then the annulus. This results in compound drops. With jets, this pattern can form composite particles, or if the annular fluid is evaporatively removed, single drops whose size is modulated by both fluids.This paper is a study of the linear temporal instability of compound threads and jets to understand how annular fluid properties control drop size in jet breakup, and to determine conditions which favour compound drop formation. The temporal dispersion equation is solved numerically for non-dimensional annular thicknesses a of order one, and analytically for thin annuli (a – 1 = ε [Lt ] 1) by asymptotic expansion in ε. There are two temporally growing modes: a stretching mode, unstable for wavelengths greater than the undisturbed inner circumference 2πR1, in which the two interfaces grow in phase; and a squeezing mode, unstable for wavelengths greater than 2πaR1, which grows exactly out of phase. Growth rates are always real, indicating that in jetting configurations disturbances convect downstream with the base velocity. For order-one thicknesses, the growth rate of the stretching mode is higher for the entire range of system parameters examined. The drop size scales with the wavenumber of the maximally growing wave (kmax). We find that for the dominant stretching mode and a = 2, variations from 0.1 to 10 in the ratios of the annulus to core viscosity, or the tension of the outer surface to that of the inner interface, can result in changes in kmax by a factor of approximately 2. However, for these changes in the system ratios, the growth rate (smax) and the ratio of the amplitude of the outer to the inner interface (Amax) for the fastest growing wave only change marginally, with Amax near one. The system appears most sensitive to the ratio of the density of the annulus to the core fluid. For a variation between 0.1 and 10, kmax again changes by a factor of 2, but Amax and smax vary more significantly with large amplitude ratios for low density ratios. The amplitude ratio of the stretching mode at the maximally growing wave (Amax) indicates whether the film or core will break first. When this ratio is near one, linear theory predicts that the core breaks with the annulus intact, forming compound drops. Except for low values of the density ratio, our results indicate that most system conditions promote compound drop formation.For thin annuli, the growth rate disparity between modes becomes even greater. In the limit ε → 0, the squeezing growth rate is roughly proportional to ε2 while the stretching mode growth rate is roughly proportional to ε0 and asymptotes to a single jet with radius R1 and tension equal to the sum of the two tensions. Thus, in this limit the growth rate and kmax are independent of the film density and viscosity. The amplitude ratio of the stretching mode becomes equal to one for all wavenumbers; so thin films break as compound drops. Our results compare favourably with previously published measurements on unstable waves in compound jets.

Aquaporin-1, a ubiquitous water channel membrane protein, is a major contributor to cell membrane osmotic water permeability. Arteries are the physiological system where hydrostatic dominates osmotic pressure differences. In the present study, we show that the walls of large conduit arteries constitute the first example where hydrostatic pressure drives aquaporin-1-mediated transcellular/transendothelial flow. We studied cultured aortic endothelial cell monolayers and excised whole aortas of male Sprague-Dawley rats with intact and inhibited aquaporin-1 activity and with normal and knocked down aquaporin-1 expression. We subjected these systems to transmural hydrostatic pressure differences at zero osmotic pressure differences. Impaired aquaporin-1 endothelia consistently showed reduced engineering flow metrics (transendothelial water flux and hydraulic conductivity). In vitro experiments with tracers that only cross the endothelium paracellularly showed that changes in junctional transport cannot explain these reductions. Percent reductions in whole aortic wall hydraulic conductivity with either chemical blocking or knockdown of aquaporin-1 differed at low and high transmural pressures. This observation highlights how aquaporin-1 expression likely directly influences aortic wall mechanics by changing the critical transmural pressure at which its sparse subendothelial intima compresses. Such compression increases transwall flow resistance. Our endothelial and historic erythrocyte membrane aquaporin density estimates were consistent. In conclusion, aquaporin-1 significantly contributes to hydrostatic pressure-driven water transport across aortic endothelial monolayers, both in culture and in whole rat aortas. This transport, and parallel junctional flow, can dilute solutes that entered the wall paracellularly or through endothelial monolayer disruptions. Lower atherogenic precursor solute concentrations may slow their intimal entrainment kinetics.