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AJP - Heart and Circulatory Physiology, Vol 272, Issue 6 2826-H2832, Copyright © 1997 by American Physiological Society
ARTICLES |
R. Maass-Moreno and C. F. Rothe
Dept. of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46202, USA.
To test the hypothesis that the hepatic sinusoidal pressure is virtually identical to the portal venous pressure (Ppv) or the abdominal vena caval pressure (Pave), microvascular pressures were measured in liver vascular networks supplied by a single portal venule near the liver surface of alpha-chloralose-urethan-anesthetized rabbits. With the use of a servo-null pressure-measuring system, the pressures in terminal portal venules, sinusoids, and initial hepatic venules averaged 5.7 +/- 0.8 (SD), 5.4 +/- 0.7, and 4.7 +/- 0.6 mmHg, respectively, relative to the middle of the right atrium. The mean Ppv was 7.7 +/- 1.1 mmHg and the Pave was 3.9 +/- 0.7 mmHg. The sinusoidal pressure (Psinu) averaged 2.33 +/- 1.04 mmHg lower than the Ppv, and 1.54 +/- 0.63 mmHg higher than the Pave. The pressure gradient across the sinusoids averaged < 1 mmHg. The fractional pressure gradient from the sinusoids to the vena cava averaged 41 +/- 15% of the total Ppv to Pave gradient. We conclude that most of the transhepatic resistance cannot be attributed to a specific vascular segment or vessel type and that sinusoidal pressures are not closely similar to either the Ppv or the Pave, as is often assumed.
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