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1 Bioengineering, University of California San Diego, La Jolla, California, United States
2 Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, New York, New York, United States
3 Chemical Engineering, The City College of New York, GSUC of CUNY, New York, New York, United States
* To whom correspondence should be addressed. E-mail: david{at}ccny.cuny.edu.
This paper measures the filtration flows through the walls of the rat aorta, pulmonary artery (PA) and inferior vena cava (IVC), vessels with very different susceptibilities to atherosclerosis, as a function of transmural pressure 
P, both with intact and denuded endothelium on the same vessel. Aortic hydraulic conductivity Lp is high at 60 mmHg, drops by ~40% by 100 mmHg and is pressure-independent to 140 mmHg. The trends are similar in the PA and IVC, dropping 42% from 10-40 mmHg and flat to 100 mmHg (PA) and dropping 33% from 10-20 mmHg and essentially flat to 60 mmHg (IVC). Endothelial removal renders Lp(P) flat; it increases Lp of the aorta by ~75%, doubles Lp of the PA and quadruples Lp of the IVC. The specific resistance (1/Lp) of the aortic endothelium is ~47% of the total resistance, i.e., the endothelium takes up ~47% of the transmural pressure drop at 100 mmHg. The PA value is 55% above 40 mmHg and the IVC value is 23% at 10 mmHg. Lps of the intact aorta, PA and IVC have magnitudes of 10-8, 10-7 and 5x10-7 cm/(s mmHg) and wall thicknesses 145.8±9.3, 78.9±3.3 and 66.1±4.1 (mean ± SD) mm. These data are consistent with the differing wall structures of the three vessels. The rat aortic Lp data are quantitatively consistent with rabbit Lp(P) (Tedgui & Lever, AJP, 247, H784-91, 1984; Baldwin & Wilson, AJP, 264, H26-32, 1993), suggesting that intimal compression under pressure loading may also play a role in Lp(P) in these other vessels. Despite experiencing very different driving transmural pressures, these three vessels' nominal transmural water fluxes are very similar, and therefore cannot alone account for their different disease susceptibilities. The differing fates of macromolecular tracers convected by these water fluxes into these vessels' walls may address this question.
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