Blood-to-Tissue Albumin Transport in Rats Subjected to Acute Hemorrhage and Resuscitation

Hemorrhage induces a rapid redistribution of protein from extravascular spaces into the blood. We studied the effects of acute, nontraumatic hemorrhage on tracer-albumin clearances into individual tissues of rats to determine if reduced protein extravasation could account for intravascular protein gain. Three groups were studied: 1) HEM animals were anesthetized with pentobarbital sodium and bled to a mean arterial pressure of 50 mmHg for 90 min; 2) HEM-RS animals were treated identical to group 1 and then resuscitated with 5% bovine serum albumin (BSA) until baseline arterial pressures were regained; 3) SHAM animals served as time controls. Hemodynamic variables were measured periodically throughout hemorrhage and clearance periods, and plasma samples were collected prior to death for protein and hormone analysis. Plasma clearance of 131I-BSA into individual tissues was measured over the final 30 min of each protocol with a terminal injection of 125I-BSA used to correct for intravascular volume. Reduction of blood volume by 35% in HEM-treated animals resulted in a marked decrease in albumin transport relative to the SHAM group (p ≤ .05) in the following tissues: skeletal muscle (−65%), skin (−49%), ileum (−75%), cecum (−66%), colon (−67%), heart (−67%), and lung (−71%). Significant changes were not observed in the remaining tissues sampled: pancreas, kidney, and cerebrum. Albumin clearances in the HEM-RS group were slightly but not significantly lower than SHAM animals except for skeletal muscle, where transport remained depressed following resuscitation. Plasma total protein mass in HEM-treated rats was greater than predicted from the amount of protein removed during hemorrhage, indicating an intravascular protein gain equivalent to 60% of amount removed. Assuming normal lymphatic flow, the magnitude of transport reduction into individual tissues can quantitatively account for the observed redistribution of plasma protein into the vascular space. The potential role of elevated plasma vasopressin and possible mechanisms of transport reduction are discussed. Reduced protein extravasation may be responsible for maintenance of transcapillary oncotic pressure gradients and circulating plasma volume after hemorrhage.