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AJP - Renal Physiology, Vol 270, Issue 2 377-F390, Copyright © 1996 by American Physiological Society
ARTICLES |
M. F. Flessner and A. Schwab
Department of Medicine, University of Rochester, New York 14620, USA.
Ascites or dialysis fluid in the peritoneal cavity causes fluid loss from the cavity to the body. Experiments in animals and in humans have shown that the fluid loss rate increases with large increments in the intraperitoneal hydrostatic pressure (Pip). We hypothesized that there is a low-threshold Pip above which this fluid loss occurs. Because the full Pip force is exerted across the abdominal wall (AW), we further hypothesized that fluid movement into the abdominal wall would vary directly with the Pip. To address these questions, we dialyzed rats for 3 h in the supine position at constant levels of Pip with isotonic and hypertonic dialysis solutions containing a protein marker of fluid movement. We measured total fluid loss, AW fluid-marker concentration, and lymph flow. With variation of Pip from 0 to 8 cmH2O, we found that 1) lymph flows (0.61 +/- 0.03 ml/h) were not dependent on Pip, 2) measured isotonic fluid loss rate varied from 0.29 +/- 0.06 ml/h at 0 cmH2O to 0.62 +/- 0.02 at 2 cmH2O and then rose in a linear fashion to 5.06 +/- 0.10 ml/h at 8 cmH2O, 3) fluid movement into the AW paralleled the measured fluid loss rate, and 4) protein clearance from the cavity overestimated the true fluid loss because of adsorption of the marker to the peritoneal surface. We conclude that, although peritoneal lymph flow is not dependent on intraperitoneal hydrostatic or osmotic pressure, fluid loss from the cavity and fluid loss to the abdominal wall are directly proportional to Pip > 2 cmH2O. We also note that protein markers of fluid movement require correction for tissue surface adsorption for accurate results.
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