Hemorrhage remains a primary cause of death in civilian and military
trauma. Permissive hypotensive
resuscitation is a possible approach to reduce
bleeding in patients until they can be stabilized in an appropriate hospital setting. Small-volume
resuscitation with hypertonic saline (HS) is of particular interest because it allows one to modulate the inflammatory response to
hemorrhage and
trauma. Here, we tested the utility of permissive hypotensive
resuscitation with hypertonic fluids in a rat model of
hemorrhagic shock. Animals were subjected to massive
hemorrhage [mean arterial pressure (MAP) = 30 - 35 mmHg for 2 h until decompensation] and partially resuscitated with a bolus dose of 4 mL/kg of 7.5% NaCl (HS), hypertonic
hydroxyl ethyl
starch (HHES;
hydroxyl ethyl
starch + 7.5% NaCl), or
normal saline (NS) followed by additional infusion of
Ringer solution to maintain MAP at 40 to 45 mmHg for 40 min (hypotensive state). Finally, animals were fully resuscitated with
Ringer solution and the heparinized shed blood. Hypotensive
resuscitation with NS caused a significant increase in plasma
interleukin (IL)-1beta,
IL-6,
IL-2,
interferon gamma (IFNgamma),
IL-10, and
granulocyte-macrophage colony stimulating factor (
GM-CSF). This increase was blocked by treatment with HS. HHES treatment significantly reduced the increase of IL-1beta and
IL-2 but not that of the other
cytokines studied. Despite the strong effects of HS and HHES on
cytokine production, both treatments had little effect on plasma
lactate, base excess (BE), white blood cell (WBC) count,
myeloperoxidase (MPO) content, and the wet/dry weight ratio of the lungs. Moreover, on day 7 after
shock, the survival rate in rats treated with HS was markedly, but not significantly, lower than that of NS-treated animals (47% vs. 63%, respectively). In summary, hypotensive
resuscitation with hypertonic fluids reduces the inflammatory response but not lung tissue damage or mortality after severe
hemorrhagic shock.