Welcome to CDC stacks | Resuscitation of traumatic hemorrhagic shock patients with hypertonic saline - without dextran - inhibits neutrophil and endothelial cell activation - 33434 | CDC Public Access
Stacks Logo
Advanced Search
Select up to three search categories and corresponding keywords using the fields to the right. Refer to the Help section for more detailed instructions.
Clear All Simple Search
Advanced Search
Resuscitation of traumatic hemorrhagic shock patients with hypertonic saline - without dextran - inhibits neutrophil and endothelial cell activation
Filetype[PDF-1.68 MB]

  • Pubmed ID:
  • Pubmed Central ID:
  • Description:

    Post-traumatic inflammation and excessive neutrophil activation cause multiple organ dysfunction syndrome (MODS), a major cause of death among hemorrhagic shock patients. Traditional resuscitation strategies may exacerbate inflammation and thus novel fluid treatments are needed to reduce these post-traumatic complications. Hypertonic resuscitation fluids inhibit inflammation and reduce MODS in animal models. Here we studied the anti-inflammatory efficacy of hypertonic fluids in a controlled clinical trial.


    Trauma patients in hypovolemic shock were resuscitated in a pre-hospital setting with 250 ml of either 7.5% hypertonic saline (HS; n=9), 7.5% hypertonic saline + 6% dextran-70 (HSD; n=8), or 0.9% normal saline (NS; n=17). Blood samples were collected on hospital admission and 12 and 24 h post-resuscitation. Multi-color flow cytometry was used to quantify neutrophil expression of cell-surface activation/adhesion (CD11b, CD62L, CD64) and degranulation (CD63, CD66b, CD35) markers as well as oxidative burst activity. Circulating concentrations of soluble intercellular adhesion molecule (sICAM)-1, vascular cell adhesion molecule (sVCAM)-1, P-, E-selectins, myeloperoxidase (MPO), and matrix metallopeptidase (MMP)-9 were assessed with immunoassays.


    MODS, leukocytosis, and mortality were lower in the HS and HSD groups than in the NS group. However, these differences were not statistically significant. HS prevented priming and activation and neutrophil oxidative burst and CD11b and CD66b expression. HS also reduced circulating markers of neutrophil degranulation (MPO and MMP-9) and endothelial cell activation (sICAM-1, cVCAM-1, sE-selectin, and sP-selectin). HSD was less capable than HS of suppressing the upregulation of most of these activation markers.


    This study demonstrates that initial resuscitation with HS but neither NS nor HSD can attenuate post-traumatic neutrophil and endothelial cell activation in hemorrhagic shock patients. These data suggest that hypertonic resuscitation without dextran may inhibit post-traumatic inflammation. However, despite this effect, neither HS nor HSD reduced MODS in trauma patients with hemorrhagic shock.

  • Document Type:
  • Collection(s):
  • Funding:
    5U01HL077863/HL/NHLBI NIH HHS/United States
    AI-072287/AI/NIAID NIH HHS/United States
    AI-080582/AI/NIAID NIH HHS/United States
    GM-51477/GM/NIGMS NIH HHS/United States
    GM-60475/GM/NIGMS NIH HHS/United States
    HL077865/HL/NHLBI NIH HHS/United States
    HL077866/HL/NHLBI NIH HHS/United States
    HL077867/HL/NHLBI NIH HHS/United States
    HL077871/HL/NHLBI NIH HHS/United States
    HL077872/HL/NHLBI NIH HHS/United States
    HL077873/HL/NHLBI NIH HHS/United States
    HL077881/HL/NHLBI NIH HHS/United States
    HL077885/HL/NHLBI NIH HHS/United States
    HL077887/HL/NHLBI NIH HHS/United States
    HL077908/HL/NHLBI NIH HHS/United States
    PR043034/PR/OCPHP CDC HHS/United States
    R01 AI072287/AI/NIAID NIH HHS/United States
    R01 AI080582/AI/NIAID NIH HHS/United States
    R01 GM051477/GM/NIGMS NIH HHS/United States
    R01 GM060475/GM/NIGMS NIH HHS/United States
    R01 GM076101/GM/NIGMS NIH HHS/United States
    R01 HL073233/HL/NHLBI NIH HHS/United States
    R29 GM051477/GM/NIGMS NIH HHS/United States
    Canadian Institutes of Health Research/Canada
No Related Documents.
You May Also Like: