Damage control resuscitation decreases systemic inflammation after hemorrhage.
BACKGROUND
Severe hemorrhagic shock and resuscitation initiates a dysfunctional systemic inflammatory response leading to end-organ injury. Clinical evidence supports the transfusion of high ratios of plasma and packed red blood cells (pRBCs) in the treatment of hemorrhagic shock. The effects of resuscitation with different ratios of fresh blood products on inflammation and organ injury have not yet been characterized.


METHODS
Mice underwent femoral artery cannulation and pressure-controlled hemorrhage for 60 min, then resuscitation with fresh plasma and pRBCs collected from donor mice. Plasma alone, pRBCs alone, and ratios of 2:1, 1:1, and 1:2 plasma:pRBCs were used for resuscitation strategies. Mice were sacrificed to determine biochemical and hematologic parameters, serum cytokine concentrations, tissue myeloperoxidase levels, and vascular permeability.


RESULTS
Compared with other resuscitation strategies, mice resuscitated with pRBCs alone exhibited increased hemoglobin levels, while other hematologic and biochemical parameters were not significantly different among groups. Compared with 1:1, mice resuscitated with varying ratios of plasma:pRBCs exhibited increased cytokine concentrations of KC, MIP-1α, and MIP-2, and increased intestinal and lung myeloperoxidase levels. Mice resuscitated with 1:1 had decreased vascular permeability in the intestine and lung as compared with other groups.


CONCLUSIONS
Resuscitation with a 1:1 ratio of fresh plasma:pRBCs results in decreased systemic inflammation and attenuated organ injury. These findings support the potential advantage of transfusing blood products in physiologic ratios to improve the treatment of severe hemorrhagic shock.
Department of Surgery, Institute of Military Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0558, USA.
Amy T
AT
Makley
Michael D
MD
Goodman
Ritha M
RM
Belizaire
Lou Ann W
LA
Friend
Jay A
JA
Johannigman
Warren C
WC
Dorlac
Alex B
AB
Lentsch
Timothy A
TA
Pritts
D000818:Animals; D054405:Chemokine CCL3 / Q000378:metabolism; D054426:Chemokine CXCL2 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D004912:Erythrocytes; D006470:Hemorrhage / Q000150:complications*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D009195:Peroxidase / Q000378:metabolism; D010949:Plasma; D012151:Resuscitation / Q000379:methods*; D012771:Shock, Hemorrhagic / Q000150:complications*; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control*; D016896:Treatment Outcome
D054405:Chemokine CCL3; D054426:Chemokine CXCL2; D018925:Chemokines; C074302:keratinocyte-derived chemokines; D009195:Peroxidase