坪田 健一

A numerical simulation was carried out to investigate the blood flow behavior (i.e., flow rate and pressure) and coupling of a renal vascular network and the myogenic response to various conditions. A vascular segment and an entire kidney vascular network were modeled by assuming one single vessel as a straight pipe whose diameter was determined by Murray’s law. The myogenic response was tested on individual AA (afferent artery)–GC (glomerular capillaries)–EA (efferent artery) systems, thereby regulating blood flow throughout the vascular network. Blood flow in the vascular structure was calculated by network analysis based on Hagen–Poiseuille’s law to various boundary conditions. Simulation results demonstrated that, in the vascular segment, the inlet pressure Pinlet and the vascular structure act together on the myogenic response of each individual AA–GC–EA subsystem, such that the early-branching subsystems in the vascular network reached the well-regulated state first, with an interval of the inlet as Pinlet = 10.5–21.0 kPa, whereas the one that branched last exhibited a later interval with Pinlet = 13.0–24.0 kPa. In the entire vascular network, in contrast to the Pinlet interval (13.0–20.0 kPa) of the unified well-regulated state for all AA–GC–EA subsystems of the symmetric model, the asymmetric model exhibited the differences among subsystems with Pinlet ranging from 12.0–17.0 to 16.0–20.0 kPa, eventually achieving a well-regulated state of 13.0–18.5 kPa for the entire kidney. Furthermore, when Pinlet continued to rise (e.g., 21.0 kPa) beyond the vasoconstriction range of the myogenic response, high glomerular pressure was also related to vascular structure, where PGC of early-branching subsystems was 9.0 kPa and of late-branching one was 7.5 kPa. These findings demonstrate how the myogenic response regulates renal blood flow in vascular network system that comprises a large number of vessel elements.

Three-dimensional computational fluid dynamics (CFD) simulations were performed in the anastomotic region of the Fontan route between the venae cava and pulmonary arteries to investigate the risk of thrombosis due to blood stasis in the Fontan circulation. The finite volume method based on the time-averaged continuity and Navier–Stokes equations combined with the k-ω SST turbulent model was used in the CFD simulations. Low shear rate (SR) and SR on the wall (WSR) of <10 s−1 were used as markers to assess blood stasis as a cause of blood coagulation. Simulated blood flow velocity and both SR and WSR were reduced in the right atrium (RA) as the cavity of a flow channel in the atriopulmonary connection (APC) Fontan model, whereas the values increased in the total cavopulmonary connection (TCPC) Fontan model, which has no cavity. The volume of SR <10 s−1 and wall surface area of WSR <10 s−1 were, respectively, 4.6–261.8 cm3 and 1.2–38.3 cm2 in the APC Fontan model, and 0.1–0.3 cm3 and 0.1–0.6 cm2 in the TCPC Fontan model. The SR and WSR increased in the APC model with a normal-sized RA and the TCPC model as the flow rate of blood from the inferior vena cava increased with exercise; however, the SR and WSR in the RA decreased in the APC model with a dilated RA owing to the development of a recirculating flow. These findings suggest that the APC Fontan has a higher risk of thrombosis due to blood stasis than the TCPC Fontan and a higher RA dilation is associated with a higher risk of thrombosis from a fluid mechanics perspective.