arXiv2026
Red blood cell (RBC) populations are mechanically and morphologically heterogeneous, yet how this heterogeneity governs transport, splenic retention and blood rheology in confinement remains unclear. We combine microchannel experiments with dissipative particle dynamics (DPD) simulations to determine how the morphology, deformability and hydrodynamic interaction of immature RBCs (reticulocytes) shape microconfined flow in acute and chronic mountain sickness. Reticulocyte-rich samples present the three shapes that the maturation literature assigns to successive reticulocyte stages -- multilobular, cup-shaped and near-discocytic -- which we model as R1-R3, each with a membrane shear modulus within the range reported for reticulocytes. A 5-um microchannel resolves these models only weakly, R1 taking at most ~18% longer than control discocytes to cross it, whereas a 1.5-um splenic slit, driven at its own loading, delays R1 by ~30%; both geometries order the models by shear modulus. In cell pairs, a leading cell never lets a follower pass below its own single-cell threshold, ruling out the order-of-magnitude reduction that a wake-"unjamming" picture would suggest; instead the follower queues behind the leader, and a stiffer leader, which clears the slit more slowly, delays it more. The controlling variable is the single-cell critical pressure gradient Delta P_c, which rises monotonically from control discocytes through the reticulocyte subtypes to sickled cells. Set against published rheograms, an analytical estimate attributes chronic-mountain-sickness hyperviscosity mainly to hematocrit-driven crowding rather than single-cell rheology. These results place benign acclimatization, chronic-mountain-sickness hyperviscosity and sickle-cell-trait splenic syndrome on a single mechanical axis defined by Delta P_c.