Pressure threshold for fluid loss from the peritoneal cavity. Flessner, Michael F. Department of Medicine, University of Rochester, Rochester, New York
APStracts 2:0148F, 1995.
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 i.p. hydrostatic pressure (IPP). We hypothesized that there is a low threshold IPP above which this fluid loss occurs. Because the full IPP force is exerted across the abdominal wall (AW), we further hypothesized that fluid movement into the abdominal wall would vary directly with the IPP. To address these questions, we dialyzed rats for 3 hours in the supine position at constant levels of IPP 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 IPP from 0 to 8 cm H2O, we found that: a) lymph flows (.61+.03 ml/h) were not dependent on IPP; b) measured isotonic fluid loss rate varied from .29+.06 ml/h at 0 cm H2O to .62+.02 at 2 cm H2O and then rose in a linear fashion to 5.06+.10 ml/h at 8 cm H2O; and c) fluid movement into the AW paralleled the measured fluid loss rate; d) protein clearance from the cavity overestimated the true fluid loss because of adsorption of the marker to the peritoneal surface. We conclude that while peritoneal lymph flow is not dependent on i.p. hydrostatic or osmotic pressure, fluid loss from the cavity and fluid loss to the abdominal wall are directly proportional to IPP above 2 cm H2O. We also note that protein markers of fluid movement require correction for tissue surface adsorption for accurate results.

Received 10 April 1995; accepted in final form 21 August 1995.
APS Manuscript Number F121-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 15 September 1995.