Microscale solute flow probed with rotating microbead trapped in optical vortex

The dynamics of solute flow in the microscopic chamber can be studied with optical tweezers. A method based on the metallic microbeads trapped in the focused optical vortex beam is proposed. This annular beam of a twisted wavefront exerts torque on a reflective object placed inside the dark core of the vortex. The induced rotational movement of the bead is sensitive to local viscosity changes in the surrounding medium, for example, during the ongoing dissolution process. Two experimental configurations are described, both relying on tracing the angular velocity of the bead in time. In one-bead configuration, the dynamics of local solute concentration can be studied. In two-bead case, the direction and speed of solute flow can be probed with a spatial resolution of single micrometers. We approach the elementary problem of sucrose dissolution and diffusion in water. The surprising impression of the reverse solute flow was observed. Further experimental investigation led to the discovery that this phenomenon originates from the sucrose stream-like diffusion in the mid-depth of the measurement chamber. The rotating microbead method applies for various solid and liquid substances and may become a useful technique for microfluidics research. Graphic abstract

A mathematical model of the rat kidney. II. Antidiuresis

Kidney water conservation requires a hypertonic medullary interstitium, NaCl in the outer medulla and NaCl and urea in the inner medulla, plus a vascular configuration that protects against washout. In this work, a multisolute model of the rat kidney is revisited to examine its capacity to simulate antidiuresis. The first step was to streamline model computation by parallelizing its Jacobian calculation, thus allowing finer medullary spatial resolution and more extensive examination of model parameters. It is found that outer medullary NaCl is modestly increased when transporter density in ascending Henle limbs from juxtamedullary nephrons is scaled to match the greater juxtamedullary solute flow. However, higher NaCl transport produces greater CO2 generation and, by virtue of countercurrent vascular flows, establishment of high medullary Pco2. This CO2 gradient can be mitigated by assuming that a fraction of medullary transport is powered anaerobically. Reducing vascular flows or increasing vessel permeabilities does little to further increase outer medullary solute gradients. In contrast to medullary models of others, vessels in this model have solute reflection coefficients close to zero; increasing these coefficients provides little enhancement of solute profiles but does generate high interstitial pressures, which distort tubule architecture. Increasing medullary urea delivery via entering vasa recta increases inner medullary urea, although not nearly to levels found in rats. In summary, 1) medullary Na+ and urea gradients are not captured by the model and 2) the countercurrent architecture that provides antidiuresis also produces exaggerated Pco2 profiles and is an unappreciated constraint on models of medullary function.