| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
1 Institute of Biocybernetics and Biomedical Engineering, Warsaw, Poland
2 Institute of Biocybernetics and Biomedical Engineering, Warsaw, Poland; Divisions of Baxter Novum and Renal Medicine, CLINTEC, Karolinska Institute, Stockholm, Sweden
3 Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, United States
4 Divisions of Baxter Novum and Renal Medicine, CLINTEC, Karolinska Institute, Stockholm, Sweden
* To whom correspondence should be addressed. E-mail: jacekwan{at}ibib.waw.pl.
The process of water reabsorption from the peritoneal cavity into the surrounding tissue substantially decreases the net ultrafiltration in patients on peritoneal dialysis. The goal of this study is to propose a mathematical model based on data from clinical studies and animal experiments in order to describe the changes in the absorption rate, interstitial hydrostatic pressure and tissue hydration caused by the increased intraperitoneal pressure after the initiation of peritoneal dialysis. The model describes water transport through a deformable, porous tissue after infusion of isotonic solution into the peritoneal cavity. Blood capillary and lymphatic vessels are assumed to be uniformly distributed within the tissue. Starling's law is applied for a description of fluid transport through the capillary wall, and the transport within the interstitium is modeled by Darcy's law. Transport parameters such as void volume, tissue hydraulic conductance, and lymphatic absorption in the tissue are dependent on the local interstitial pressure. Numerical simulations show the strong dependency of fluid absorption and tissue hydration on the values of intraperitoneal pressure. Our results predict that in the steady state only about 20-40% of the fluid, which flows into the tissue from peritoneal cavity, is absorbed by the lymphatics situated in the tissue, whereas the larger (60-80%) part of the fluid is absorbed by the blood capillaries.
This article has been cited by other articles:
|
|
 |
|
  Y.-L. Kim, S.-H. Park, J.-Y. Choi, and C.-D. Kim Cyclooxygenase-2 inhibitor: a potential therapeutic strategy for ultrafiltration failure in peritoneal dialysis Nephrol. Dial. Transplant., December 1, 2009; 24(12): 3585 - 3588. [Full Text] [PDF]
|
|
|
|
 |
|
 J. Waniewski, M. Debowska, and B. Lindholm WATER AND SOLUTE TRANSPORT THROUGH DIFFERENT TYPES OF PORES IN PERITONEAL MEMBRANE IN CAPD PATIENTS WITH ULTRAFILTRATION FAILURE Perit. Dial. Int., November 1, 2009; 29(6): 664 - 669. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Waniewski, J. Stachowska-Pietka, and M. F. Flessner Distributed modeling of osmotically driven fluid transport in peritoneal dialysis: theoretical and computational investigations Am J Physiol Heart Circ Physiol, June 1, 2009; 296(6): H1960 - H1968. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. F. Flessner Distributed model of peritoneal transport: implications of the endothelial glycocalyx Nephrol. Dial. Transplant., July 1, 2008; 23(7): 2142 - 2146. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
