Hemorrhage induces a rapid redistribution of protein from extravascula
r spaces into the blood. We studied the effects of acute, nontraumatic
hemorrhage on tracer-albumin clearances into individual tissues of ra
ts to determine if reduced protein extravasation could account for int
ravascular protein gain. Three groups were studied: 1) HEM animals wer
e anesthetized with pentobarbital sodium and bled to a mean arterial p
ressure of 50 mmHg for 90 min; 2) HEM-RS animals were treated identica
l to group 1 and then resuscitated with 5% bovine serum albumin (BSA)
until baseline arterial pressures were regained; 3) SHAM animals serve
d as time controls. Hemodynamic variables were measured periodically t
hroughout hemorrhage and clearance periods, and plasma samples were co
llected prior to death for protein and hormone analysis. Plasma cleara
nce of I-131-BSA into individual tissues was measured over the final 3
0 min of each protocol with a terminal injection of I-125-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 less than or equal to.05) in the follow
ing tissues: skeletal muscle (-65%), skin (-49%), ileum (-75%), cecum
(-66%), colon (-67%), heart (-67%), and lung (-71%). Significant chang
es were not observed in the remaining tissues sampled: pancreas, kidne
y, and cerebrum. Albumin clearances in the HEM-RS group were slightly
but not significantly lower than SHAM animals except for skeletal musc
le, where transport remained depressed following resuscitation. Plasma
total protein mass in HEM-treated rats was greater than predicted fro
m the amount of protein removed during hemorrhage, indicating an intra
vascular protein gain equivalent to 60% of amount removed. Assuming no
rmal lymphatic flow, the magnitude of transport reduction into individ
ual tissues can quantitatively account for the observed redistribution
of plasma protein into the vascular space. The potential role of elev
ated plasma vasopressin and possible mechanisms of transport reduction
are discussed. Reduced protein extravasation may be responsible for m
aintenance of transcapillary oncotic pressure gradients and circulatin
g plasma volume after hemorrhage.