Impairment of blood volume restitution after large hemorrhage: a
mathematical model.
Carlson, Drew E., Mark D. Kligman, and Donald S. Gann.
Departments of Surgery and Physiology, University of Maryland
School of Medicine, Baltimore, Maryland 21201
APStracts 2:0354R, 1995.
Impairment of blood volume restitution after large hemorrhage: a
mathematical model. Am. J. Physiol. (Regulatory Integrative Comp.
Physiol.), 1994. A mathematical model tests possible mechanisms for
the progressive failure of blood volume restitution seen after larger
hemorrhages (>26%) with increasing changes in plasma osmolality.
After 10% hemorrhage, the model requires a decrease in net
hydrostatic capillary pressure, the release of solute into the
extracellular space, and the release of Na+ and K+ from a bound pool
in equilibrium with the interstitium to match the experimental data.
The solute and released cations expand the interstitium to drive the
restitution of volume and protein from 3 to 24 h. After 30%
hemorrhage the best prediction of the average experimental responses
occurs when the Na, K-ATPase in the cell membrane is inhibited by
38.7% from 0.8 to 3 h and the proportionality between capillary
pressure and blood volume is reduced by 68% from its value for 10%
hemorrhage. When the change in plasma osmolality is doubled after 30%
hemorrhage, an increase in the inhibition of the ATPase to 85% and
extension of its duration to 24 h is necessary to match experimental
findings. The associated defect in sodium transport may occur after
large hemorrhage, so that sodium and water move into cells. This
response may oppose osmotically-driven expansion of the interstitium
and thus account for the failure of restitution.
Received 18 November 1994; accepted in final form 4 December
1995.
APS Manuscript Number R666-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95