Resuscitation with a blood substitute abrogates pathologic postinjury neutrophil cytotoxic function.

BACKGROUND Resuscitation with oxygen-carrying fluids is critically important in the patient with hemorrhagic shock caused by trauma. However, it is clear that a number of biologic mediators present in stored blood (packed red blood cells [PRBCs]) have the potential to exacerbate early postinjury hyperinflammation and multiple organ failure through priming of circulating neutrophils (PMNs). PolyHeme (Northfield Laboratories, Evanston, IL), a hemoglobin-based substitute that is free of priming agents, provides an alternative. We hypothesized that PMN priming would be attenuated in patients resuscitated with PolyHeme in lieu of stored blood. METHODS Injured patients requiring urgent transfusion were given either PolyHeme (up to 20 units) or PRBCs. Early postinjury PMN priming was measured via beta-2 integrin expression, superoxide production, and elastase release. RESULTS Treatment groups were comparable with respect to extent of injury and early physiologic compromise. PMNs from patients resuscitated with PRBCs showed priming in the early postinjury period by all three measures. No such priming was evident in patients resuscitated with PolyHeme. CONCLUSION The use of a blood substitute in the early postinjury period avoids PMN priming and may thereby provide an avenue to decrease the incidence or severity of postinjury multiple organ failure.

[1]  E. Moore,et al.  Age of transfused blood is an independent risk factor for postinjury multiple organ failure. , 1999, American journal of surgery.

[2]  E. Moore,et al.  The first randomized trial of human polymerized hemoglobin as a blood substitute in acute trauma and emergent surgery. , 1998, Journal of the American College of Surgeons.

[3]  N. Voelkel,et al.  Plasma and lipids from stored packed red blood cells cause acute lung injury in an animal model. , 1998, The Journal of clinical investigation.

[4]  E. Moore,et al.  Clinical utility of human polymerized hemoglobin as a blood substitute after acute trauma and urgent surgery. , 1997, The Journal of trauma.

[5]  I. T. Demchenko,et al.  Blood flow regulation by S-nitrosohemoglobin in the physiological oxygen gradient. , 1997, Science.

[6]  A. Sauaia,et al.  Blood Transfusion: An Independent Risk Factor for Postinjury Multiple Organ Failure , 1997 .

[7]  M. Fujihara,et al.  Generation of interleukin 8 in stored apheresis platelet concentrates and the preventive effect of prestorage ultraviolet B radiation , 1997, Transfusion.

[8]  C. Haslett,et al.  Demonstration of reversible priming of human neutrophils using platelet-activating factor. , 1996, Blood.

[9]  A. Sauaia,et al.  The inflammatory profile of interleukin-6, interleukin-8, and soluble intercellular adhesion molecule-1 in postinjury multiple organ failure , 1996 .

[10]  F. A. Moore,et al.  Sequential systemic platelet‐activating factor and interleukin 8 primes neutrophils in patients with trauma at risk of multiple organ failure , 1996, The British journal of surgery.

[11]  E. Deitch,et al.  Role of the Gut in Multiple Organ Failure: Bacterial Translocation and Permeability Changes , 1996, World Journal of Surgery.

[12]  E. Moore,et al.  Evolving concepts in the pathogenesis of postinjury multiple organ failure. , 1995, The Surgical clinics of North America.

[13]  G. Stack,et al.  Cytokine generation in stored, white cell‐reduced, and bacterially contaminated units of red cells , 1995, Transfusion.

[14]  E. Moore,et al.  The postischemic gut serves as a priming bed for circulating neutrophils that provoke multiple organ failure. , 1994, The Journal of trauma.

[15]  C. Silliman,et al.  Partial characterization of lipids that develop during the routine storage of blood and prime the neutrophil NADPH oxidase. , 1994, The Journal of laboratory and clinical medicine.

[16]  E. Abraham,et al.  Elevated levels of soluble ICAM-1 correlate with the development of multiple organ failure in severely injured trauma patients. , 1994, The Journal of trauma.

[17]  D. Heney,et al.  Increased circulating adhesion molecule concentrations in patients with the systemic inflammatory response syndrome: A prospective cohort study , 1994, Critical care medicine.

[18]  E. Snyder,et al.  Cytokine generation in stored platelet concentrates , 1994, Transfusion.

[19]  M. Cuesta,et al.  Risk factors for multiple organ system failure and death in critically injured patients. , 1993, Surgery.

[20]  E. Moore,et al.  Effects of accidental trauma on cytokine and endotoxin production. , 1993, Critical care medicine.

[21]  G. Bulkley Free radicals and other reactive oxygen metabolites: clinical relevance and the therapeutic efficacy of antioxidant therapy. , 1993, Surgery.

[22]  A. Baue The horror autotoxicus and multiple-organ failure. , 1992, Archives of surgery.

[23]  D. W. Nelson,et al.  Primed neutrophils injure rat lung through a platelet-activating factor-dependent mechanism. , 1991, The Journal of surgical research.

[24]  R. Maier,et al.  Superoxide production by neutrophils in a model of adult respiratory distress syndrome. , 1988, Archives of surgery.

[25]  G. Moss,et al.  Hemoglobin solution--from tetramer to polymer. , 1984, Surgery.

[26]  W. Shoemaker,et al.  Hemoglobin solution in the treatment of hemorrhagic shock , 1982, Critical care medicine.

[27]  A. Sauaia,et al.  Early predictors of postinjury multiple organ failure. , 1994, Archives of surgery.