Papers Published
Abstract:
Flow in arterioles is determined by a number of interacting factors, including perfusion pressure, neural stimulation, vasoactive substances, the intrinsic contractility of arteriolar walls, and wall shear stress. We have developed a two-dimensional model of arteriolar fluid flow and mass transport. The model includes a phenomenological representation of the myogenic response of the arteriolar wall, in which an increase in perfusion pressure stimulates vasoconstriction. The model also includes the release, advection, diffusion, degradation, and dilatory action of nitric oxide (NO), a potent, but short-lived, vasodilatory agent. Parameters for the model were taken primarily from the experimental literature of the rat renal afferent arteriole. Solutions to the incompressible Navier-Stokes equations were approximated by means of a splitting that used upwind differencing for the inertial term and a spectral method for the viscous term and incompressibility condition. The immersed boundary method was used to include the forces arising from the arteriolar walls. The advection of NO was computed by means of a high-order flux-corrected transport scheme; the diffusion of NO was computed by a spectral solver. Simulations demonstrated the efficacy of the numerical methods employed, and grid refinement studies confirmed anticipated first-order temporal convergence and demonstrated second-order spatial convergence in key quantities. By providing information about the effective width of the immersed boundary and sheer stress magnitude near that boundary, the grid refinement studies indicate the degree of spatial refinement required for quantitatively reliable simulations. Owing to the dominating effect of NO advection, relative to degradation and diffusion, simulations indicate that NO has the capacity to produce dilation along the entire length of the arteriole. © 1998 Academic Press.