Inversion of hematocrit partition at microfluidic bifurcations

TL;DR

This study uses microfluidic models and experiments to explore how red blood cell deformability and vessel geometry influence hematocrit partitioning at bifurcations, revealing unexpected behaviors that impact microcirculatory function.

Contribution

It uncovers the dependence of hematocrit partitioning on RBC deformability and geometry, challenging the traditional Zweifach-Fung effect with novel inverse partitioning phenomena.

Findings

Hematocrit partition depends strongly on RBC deformability for $\,<20 ext{%}$.

Inverse hematocrit partitioning observed at low hematocrit levels.

RBC organization upstream influences partitioning behavior.

Abstract

Partitioning of red blood cells (RBCs) at the level of bifurcations in the microcirculatory system affects many physiological functions yet it remains poorly understood. We address this problem by using T-shaped microfluidic bifurcations as a model. Our computer simulations and in vitro experiments reveal that the hematocrit ($\phi_0$) partition depends strongly on RBC deformability, as long as $\phi_0 <20$% (within the normal range in microcirculation), and can even lead to complete deprivation of RBCs in a child branch. Furthermore, we discover a deviation from the Zweifach-Fung effect which states that the child branch with lower flow rate recruits less RBCs than the higher flow rate child branch. At small enough $\phi_0$, we get the inverse scenario, and the hematocrit in the lower flow rate child branch is even higher than in the parent vessel. We explain this result by an intricate up-stream RBC organization and we highlight the extreme dependence of RBC transport on geometrical and cell mechanical properties. These parameters can lead to unexpected behaviors with consequences on the microcirculatory function and oxygen delivery in healthy and pathological conditions.