The goal of this study is to quantitatively describe the remodeling of the zero-stress state of the femoral artery in flow overload. Increased blood flow, approximately as a unit step change, was imposed on the femoral artery by making an arteriovenous (a-v) fistula with the epigastric vein. The a-v fistula was created in the right leg of 36 rats, which were divided equally into six groups (2 days and 1, 2, 4, 8, and 12 wk after the fistula). The vessels in the left leg were used as controls without operative trauma. The in vivo blood pressure, flow, and femoral outer diameter and the in vitro zero-stress state geometry were measured. The in vivo shear rate at the endothelial surface increased approximately as a step function by approximately 83%, after 2 days, compared with the control artery. The arterial luminal and wall area significantly increased postsurgically from 0.15 +/- 0.02 and 0.22 +/- 0.02 mm(2) to 0.28 +/- 0.04 and 0.31 +/- 0.05 mm(2), respectively, after 12 wk. The wall thickness did not change significantly over time (P > 0.1). The opening angle decreased to 82 +/- 4.2 degrees postsurgically when compared with controls (102 +/- 4.4) after 12 wk and correlated linearly with the thickness-to-radius ratio. Histological analysis revealed vascular smooth muscle cell growth. The remodeling data are expressed mathematically in terms of indicial functions, i.e., change of a particular feature of a blood vessel in response to a unit step change of blood flow. The indicial function approach provides a quantitative description of the remodeling process in the blood vessel wall.
A force measurement device has been designed to monitor the mechanical properties of fracture site with external fixation. Forces are measured through electric resistance strain gauges mounted on fixation framework and the measurement results are displayed on an LCD screen. The device features a force range of 0-10 kg with linearity and repeatability less than 1% and accuracy less than 0.1 kg.
We measured the Fahraeus effect of blood flowing in a sheet flow model formed with two glass slides. The number of red blood cells in the sheet flow was counted to determine a sheet hematocrit Hs and the discharge hematocrit Hd was measured from blood collection. For a Hd in the range of 3 to 30 percent, we find that Hs/Hd is about .83 for a gap of 4.1 microns. When the discharge hematocrit is 30 percent, the ratio decreases to .66 as the gap approaches 7 microns and then increases as the gap becomes thicker. The results indicate that the hematocrit ratio for a gap thicker than 4.1 microns is an increasing function of the discharge hematocrit. The value of Hs/Hd found for the sheet flow models and its dependence on Hd are comparable to those of circular tubes when their diameter equals the gap thickness.
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