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Logo of bmcgastBioMed Centralsearchsubmit a manuscriptregisterthis articleBMC Gastroenterology
 
BMC Gastroenterol. 2012; 12: 26.
Published online Mar 27, 2012. doi:  10.1186/1471-230X-12-26
PMCID: PMC3361476
Quantitative modeling of the physiology of ascites in portal hypertension
David G Levittcorresponding author1 and Michael D Levitt2
1Department of Integrative Biology and Physiology, University of Minnesota, 6-125 Jackson Hall, 321 Church St. S. E., Minneapolis, MN 55455, USA
2Research Service, Veterans Affairs Medical Center, VAMC/111D, 1 Veterans Drive, Minneapolis, MN 55417, USA
corresponding authorCorresponding author.
David G Levitt: levit001/at/umn.edu; Michael D Levitt: michael.levitt/at/va.gov
Received December 15, 2011; Accepted March 27, 2012.
Abstract
Although the factors involved in cirrhotic ascites have been studied for a century, a number of observations are not understood, including the action of diuretics in the treatment of ascites and the ability of the plasma-ascitic albumin gradient to diagnose portal hypertension. This communication presents an explanation of ascites based solely on pathophysiological alterations within the peritoneal cavity. A quantitative model is described based on experimental vascular and intraperitoneal pressures, lymph flow, and peritoneal space compliance. The model's predictions accurately mimic clinical observations in ascites, including the magnitude and time course of changes observed following paracentesis or diuretic therapy.
Keywords: Ascites, Cirrhosis, Portal hypertension, Wedge pressure
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