Pathways and densities of descending vasa recta (DVR) and ascending vasa recta (AVR) in the outer zone of the inner medulla (IM) were evaluated to better understand medullary countercurrent exchange. Nearly all urea transporter B (UT-B)-positive DVR, those vessels exhibiting a continuous endothelium, descend with little or no branching exclusively through the intercluster region. All DVR have a terminal fenestrated (PV-1-positive) segment that partially overlaps with the UT-B-positive segment. This fenestrated segment descends a distance equal to approximately 15% of the length of the connecting UT-B-positive segment before formation of the first branch. The onset of branching is indicative of vessel entry into the intracluster region. The number density of UT-B-positive DVR at 3,000 mum below the OM-IM boundary is approximately 60% lower than the density at 400 mum below the OM-IM boundary, a result of DVR joining to fenestrated interconnecting vessels and an overall decline in UT-B expression. AVR that lie in the intercluster region (designated AVR(2)) lie distant from CDs and ascend to the OM-IM boundary with little or no branching. AVR(2a) represent a subcategory of AVR(2) that abut DVR. The mean DVR length (combined UT-B- and PV-1-positive segments) nearly equals the mean AVR(2a) length, implying a degree of overall equivalence in fluid and solute countercurrent exchange may exist. The AVR(2)/DVR ratio is approximately 2:1, and the AVR(2a)/DVR ratio is approximately 1:1; however, the AVR/DVR ratio determined for the full complement of fenestrated vessels is approximately 4:1. The excess fenestrated vessels include vessels of the intracluster region (designated AVR(1)). Countercurrent exchange between vasa recta occurs predominantly in the intercluster region. This architecture supports previous functional estimates of capillary fluid uptake in the renal IM.

Posterior tibial tendon dysfunction (PTTD) is a common degenerative condition leading to a severe impairment of gait. There is currently no effective method to determine whether a patient with advanced PTTD would benefit from several months of bracing and physical therapy or ultimately require surgery. Tendon degeneration is closely associated with irreversible degradation of its collagen structure, leading to changes to its mechanical properties. If these properties could be monitored in vivo, they could be used to quantify the severity of tendonosis and help determine the appropriate treatment. The goal of this cadaveric study was, therefore, to develop and validate ultrasound elasticity imaging (UEI) as a potentially noninvasive technique for quantifying tendon mechanical properties. Five human cadaver feet were mounted in a materials testing system (MTS), while the posterior tibial tendon (PTT) was attached to a force actuator. A portable ultrasound scanner collected 2-D data during loading cycles. Young’s modulus was calculated from the strain, loading force, and cross-sectional area of the PTT. Average Young’s modulus for the five tendons was (0.45 ± 0.16 GPa) using UEI, which was consistent with simultaneous measurements made by the MTS across the whole tendon (0.52 ± 0.18 GPa). We also calculated the scaling factor (0.12 ± 0.01) between the load on the PTT and the inversion force at the forefoot, a measurable quantity in vivo. This study suggests that UEI could be a reliable in vivo technique for estimating the mechanical properties of the PTT, and as a clinical tool, help guide treatment decisions for advanced PTTD and other tendinopathies.

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Functional architecture of descending and ascending vasa recta (DVR, AVR) was examined between 0.3 and 3.0 mm below the outer‐inner medullary (OM‐IM) boundary to investigate countercurrent exchange and blood flow. All UT‐B‐positive DVR (DVRUTB) lie between CD clusters, in the intercluster region (compartment one). 75% of DVRUTB have terminal fenestrated extensions that descend 16 ± 3% of the length of the contiguous DVRUTB prior to formation of the first branch. This branch point is indicative of vessel entry into the intracluster region (compartment two), the region dominated by CDs. We distinguish AVR as fenestrated vessels that lie in the intercluster region and that do not abut CDs and do abut DVR (AVR1) or that abut neither CDs nor DVR (AVR2; AVR1+2 mean length ~1.5 mm). These contrast with fenestrated vessels that lie in the intracluster region and abut CDs (AVR3; mean length ~0.6 mm). The AVR1:DVRUTB ratio is ~1.0, the AVR2:DVRUTB ratio is ~1.8, and the ratio for the full complement of vessels is ~4.0. For each vascular bundle, AVR1+2 arise from the intracluster region about 500 μm deeper than the depth to which DVRUTB descend. AVR3 link DVR with AVR1+2, and AVR3 provide a direct pathway for fluid/solute uptake from CDs as they ascend within the CD cluster. Some proportion of AVR3 pass directly into the OM, distant from vascular bundles. A two compartment model supports multiple modes of IM blood flow regulation. DK16294