IMPAIRMENT OF BLOOD-VOLUME RESTITUTION AFTER LARGE HEMORRHAGE - A MATHEMATICAL-MODEL

A mathematical model tests possible mechanisms for the progressive fai lure of blood volume restitution seen after larger hemorrhages (> 26%) with increasing changes in plasma osmolality. After 10% hemorrhage, t he model requires a decrease in net hydrostatic capillary pressure, th e release of solute into the extracellular space, and the release of N a+ and K+ from a bound pool in equilibrium with the interstitium to ma tch 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 experim ental responses occurs when the Na+-K+-adenosinetriphosphatase (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 o smolality is doubled after 30% hemorrhage, an increase in the inhibiti on of the ATPase to 85% and extension of its duration to 24 h are nece ssary to match experimental findings. The associated defect in sodium transport may occur after large hemorrhage so that sodium and water mo ve into cells. This response may oppose osmotically driven expansion o f the interstitium and thus account for the failure of restitution.