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Hemorrhagic shock (HS) is the major leading cause of death after trauma,[1] condition with a limited therapeutic option. Fluid, blood, and its component and stopping of bleeders have been the cornerstone of management since many decades. A Recent study showed that recombinant human activated protein C, interleukin-1 (IL-1) receptor antagonist, anti-tumor necrosis factors (TNF) or anti-lipopolysaccharides agents, or tight glycemia control were tested for treatment of HS. However, these treatments were not effective and sometimes dangerous.[1] Finfer et al. reported that resuscitation with fluids and blood products induces reperfusion ischemia due to the production of reactive oxygen species and activation of immune cells.[2] The excessive release of inflammatory cytokines contributes to the tissue damage. The present study has shown that HS-induced inflammation leads to drastic changes in active cytokine milieu. Pro- and anti-inflammatory cytokines (TNF-α, IL-6, IL-10, and IL-8) and monocyte chemoattractant protein-1 are thought to be an important role in immune dysfunction resulting multi-organ failure (MOF) and death.[3] It also causes hematopoietic progenitor cells (HPCs: Colony forming unit [CFU-E], burst forming unit [BFU-E], CFU-granulocyte-monocyte/macrophage [CFU-GM]) apoptosis which leads to MOF, following severe injuries and HS in human and animal models.[4,5]

indian journal of critical care medicine/indian journal of critical care medicine

Cytokines, granulocyte-monocyte colony stimulating factor, interleukin-3 and erythropoietin: Can be a therapeutic option for the stimulation of hematopoietic progenitor cells in trauma-hemorrhagic shock?