Small-volume fluid resuscitation with hypertonic saline prevents inflammation but not mortality in a rat model of hemorrhagic shock

Soheyl Bahrami, Klaus Zimmermann, Z. Szelényi, J. Hamar, Friedrich Scheiflinger, Heinz Redl, Wolfgang G. Junger

Research output: Contribution to journalArticle

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Abstract

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)-1β, IL-6, IL-2, interferon γ (IFNγ), 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-1β 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.

Original languageEnglish
Pages (from-to)283-289
Number of pages7
JournalShock
Volume25
Issue number3
DOIs
Publication statusPublished - Mar 2006

Fingerprint

Hemorrhagic Shock
Resuscitation
Inflammation
Mortality
Hemorrhage
Interleukin-1
Starch
Hydroxyl Radical
Interleukin-2
Arterial Pressure
Cytokines
Lung
Wounds and Injuries
Granulocyte-Macrophage Colony-Stimulating Factor
Leukocyte Count
Interleukin-10
Interferons
Peroxidase
Cause of Death
Shock

Keywords

  • Hemorrhagic shock
  • Hetastarch
  • Hextend
  • Hypertonic saline fluids
  • Hypotensive resuscitation
  • Inflammation

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Physiology

Cite this

Small-volume fluid resuscitation with hypertonic saline prevents inflammation but not mortality in a rat model of hemorrhagic shock. / Bahrami, Soheyl; Zimmermann, Klaus; Szelényi, Z.; Hamar, J.; Scheiflinger, Friedrich; Redl, Heinz; Junger, Wolfgang G.

In: Shock, Vol. 25, No. 3, 03.2006, p. 283-289.

Research output: Contribution to journalArticle

Bahrami, Soheyl ; Zimmermann, Klaus ; Szelényi, Z. ; Hamar, J. ; Scheiflinger, Friedrich ; Redl, Heinz ; Junger, Wolfgang G. / Small-volume fluid resuscitation with hypertonic saline prevents inflammation but not mortality in a rat model of hemorrhagic shock. In: Shock. 2006 ; Vol. 25, No. 3. pp. 283-289.
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