Takayoshi Fukushima

Visualization and finite element analysis of pulsatile flow in models of the abdominal aortic aneurysm

Pulsatile flows in glass models simulating fusiform and lateral saccular aneurysms were investigated by a flow visualization method. When resting fluid starts to flow, the initial fluid motion is practically irrotational. After a short period of time, the flow began to separate from the proximal wall of the aneurysm. Then the separation bubble or vortex grew rapidly in size and filled the whole area of the aneurysm circumferentially. During this period of time, the center of the vortex moved from the proximal end to the distal point of the aneurysm. The transient reversal flow, for instance, which may occur at the end of the ejection period, passed between the wall of the aneurysm and the centrally located vortex. When the rate and pulsatile frequency of flow were high, the vortex broke down into highly disturbed flow (or turbulence) at the distal portion of the aneurysm. The same effect was observed when the length of the aneurysm was increased. A reduction in pulsatile amplitude made the flow pattern close to that in steady flow. A finite element analysis was made to obtain velocity and pressure fields in pulsatile flow through a tube with an axisymmetric expansion. Calculations were performed with the pulsatile flows used in the visualization experiment in order to study the effects of change in the pulsatile wave form by keeping the time-mean Reynolds number and Womersleys parameter unchanged. Calculated instantaneous patterns of velocity field and stream lines agreed well with the experimental results. The appearance and disappearance of the vortex in the dilated portion and its development resulted in complex distributions of pressure and shear fields. Locally minimum and maximum values of wall shear stress occurred at points just upstream and downstream of the distal end of the expansion when the flow rate reached its peak.

Numerical Analysis of Blood Flow in the Vertebral Artery

Abnormal hemodynamic forces associated with distortions of blood vessel lumen have been thought to play an important role in the pathogenesis of focal vascular lesions. In the vertebral artery, segments located between osseous rings are ectatic compared with those surrounded by the rings. Based on the assumption that arterial blood flow was quasi-steady, this work was undertaken to investigate the structure of flow through arterial models with one or two sinusoidal stenoses. Numerical analysis was performed by an integral-momentum method. The validity of the method was examined by comparison of experimental data so far reported with theoretical results. Velocity and wall shear stress distributions were explored in a model with two stenoses simulating a part of the vertebral artery. The ectatic segments of the vertebral artery have been known as predilection sites for atherosclerotic lesions. The present study suggested that the ectatic wall was under unstable shear stresses, the direction of which was dependent upon the magnitude of the Reynolds number.

Characteristics of secondary flow in steady and pulsatile flows through a symmetrical bifurcation

Steady and pulsatile flow in a glass model simulating an arterial bifurcation was investigated by flow visualization techniques. Secondary flow generated at the bifurcation has a similar pattern to a vortex, called the horseshoe vortex, produced around a wall-based protuberance in a circular tube. The same flow disturbance was clearly observed during the decelerating phase of pulsatile flow. The vortex produces a stagnation point on the top and bottom wall just upstream from the bifurcation apex. When aluminium dust was suspended in the test fluid perfusing the blood vessel model, particles deposited over an area spreading from the stagnation point to the lateral corners of the bifurcation. Comparison between the present results and topographical patterns of atherosclerosis reported in the literature suggests that it is in such low shear regions that lipid deposition tends to occur most.

Vortex Generation in Pulsatile Flow Through Arterial Bifurcation Models Including the Human Carotid Artery

Visualization experiments were performed to elucidate the complicated flow pattern in pulsatile flow through arterial bifurcations. Human common carotid arteries, which were made transparent, and glass-models simulating Y- and T-shaped bifurcations were used. Pulsatile flow with wave forms similar to those of arterial flow was generated with a piston pump, elastic tube, airchamber, and valves controlling the outflow resistance. Helically recirculating flow with a pattern similar to that of the horseshoe vortex produced around wall-based protuberances in circular tubes was observed in pulsatile flow through all the bifurcations used in the present study. This flow type, which we shall refer to as the horseshoe vortex, has also been demonstrated to occur at the human common carotid bifurcation in steady flow with Reynolds numbers above 100. Time-varying flows also produced the horseshoe vortex mostly during the decelerating phase. Fluid particles of dye solution approaching the bifurcation apex diverged, divided into two directions perpendicularly, and then showed helical motion representing the horseshoe vortex formation. While this helical flow was produced, the stagnation points appeared on the wall upstream of the apex. Their position was dependent upon the flow distribution ratio between the branches in the individual arteries. The region affected by the horseshoe vortex was smaller during pulsatile flow than during steady flow. Lowering the Reynolds number together with the Womersley number weakened the intensity of helical flow. A separation bubble, resulting from the divergence or wall roughness, was observed at the outer or inner wall of the branch vessels and made the flow more complicated.

Disturbance of blood flow as a factor of thrombus formation

Abstract A model study was undertaken to investigate disturbances of blood flow through stenotic blood vessels. Both axisymmetric and non-symmetric models, having different diameter ratios of constriction, were used. A sudden decrease in the critical Reynolds number took place as the degree of axisymmetric constriction increased. Two symmetrical standing eddies were noticed within the separated region behind a hemispherical bulge projecting into the boundary layer. Increase in Reynolds number resulted in the formation of secondary flow, the horse-shoe vortex. A striking feature of a pulsatile laminar flow through a circular cylinder was the appearance of reverse flow near the wall at the end of the decelerating phase. The presence of axisymmetric constriction caused pulsatile disturbances. Pulsation seemed to facilitate not only the production of vortices but also the backward spread of turbulence.

Distribution and Endothelial Morphology of Atherosclerotic Lesions at Bifurcations and Curves of Human Cerebral Arteries

The present study was an attempt to clarify mechanisms related to the development of atherosclerotic lesions at branches and curves in the human arterial tree. The distribution of atherosclerotic lesions, including cloudy thickenings, fatty streaks, fibrous plaques and complicated lesions, was investigated at bifurcations and curves of cerebral branches of the internal carotid artery. Morphological changes of the endothelium over fibrous plaques at bifurcations was also assessed, by means of scanning electron microscopy. Early atherosclerotic lesions occurred predominantly at the outer walls of bifurcations and distal to the center of the inner curvature at curves, where wall shear stress is considered to be low. In contrast, the flow divider of bifurcations and the outer curvature of the bends, presumably high-shear regions, were free of early lesions. Endothelial cells over fibrous plaques without sudanophilia(FP) and with sudanophilia(SP) were significantly less elongated than those in lesion-free areas. In addition, endothelial cells over the FP and SP showed significantly more microvillous projections than did those in lesion-free areas. These results suggest that focal hemodynamic forces are implicated in the development of the atherosclerotic lesions.