The proposed Career Development Award project will provide the Candidate, Timothy A. Pritts, MD, PhD, a vehicle to attain full independence as a scientific investigator. Dr. Pritts'immediate and long term research goals are to become an independent surgeon scientist investigating the pathophysiology of hemorrhagic shock and resuscitation. The proposed research project involves hemorrhagic shock, a major cause of death and disability. Recent innovations in clinical care have been proposed as an attempt to improve immediate survival. Termed """"""""damage control resuscitation,"""""""" these strategies emphasize liberal transfusion of plasma and red blood cells. Early retrospective data suggest that increasing ratios of plasma to red blood cells leads to decreased immediate mortality in trauma patients but may allow subsequent death from multiple organ failure. To date, there are no studies examining the impact of damage control resuscitation strategies, as compared to traditional resuscitation, on subsequent development of SIRS, organ failure, and death. The proposed studies will use a murine model of hemorrhagic shock and resuscitation to directly compare resuscitation with crystalloid fluids, whole blood, and varying ratios of plasma to red blood cells on the development of systemic inflammation, organ failure, and death. The Career Development Plan will involve active mentoring by Alex Lentsch, PhD, as well as oversight by an advisory committee, diminution of clinical and administrative activities, and additional training in immunology. The research environment in the Department of Surgery is outstanding, with well equipped facilities and all necessary equipment to complete the proposed experiments. Dr. Pritts enjoys the complete support of his Chair, his Division Director, and the Department.
Hemorrhagic shock is a major cause of death in injured patients. Strategies to improve resuscitation and survival from hemorrhagic shock are evolving. The proposed experiments will increase understanding of the mechanisms of different resuscitation strategies for patients who are victims of hemorrhagic shock.
|Sutton, Jeffrey M; Pritts, Timothy A (2014) Human beta-defensin 3: a novel inhibitor of Staphylococcus-produced biofilm production. Commentary on ""Human *-defensin 3 inhibits antibiotic-resistant Staphylococcus biofilm formation"". J Surg Res 186:99-100|
|Richter, Jillian R; Sutton, Jeffrey M; Belizaire, Ritha M et al. (2014) Macrophage-derived chemokine (CCL22) is a novel mediator of lung inflammation following hemorrhage and resuscitation. Shock 42:525-31|
|Yang, Sung H; Gangidine, Matt; Pritts, Timothy A et al. (2013) Interleukin 6 mediates neuroinflammation and motor coordination deficits after mild traumatic brain injury and brief hypoxia in mice. Shock 40:471-5|
|Huber, Nathan L; Bailey, Stephanie R; Schuster, Rebecca et al. (2012) Prior thermal injury accelerates endotoxin-induced inflammatory cytokine production and intestinal nuclear factor-?B activation in mice. J Burn Care Res 33:279-85|
|Belizaire, Ritha M; Makley, Amy T; Campion, Eric M et al. (2012) Resuscitation with washed aged packed red blood cell units decreases the proinflammatory response in mice after hemorrhage. J Trauma Acute Care Surg 73:S128-33|
|Belizaire, Ritha M; Prakash, Priya S; Richter, Jillian R et al. (2012) Microparticles from stored red blood cells activate neutrophils and cause lung injury after hemorrhage and resuscitation. J Am Coll Surg 214:648-55; discussion 656-7|
|Sonnier, Dennis I; Bailey, Stephanie R; Schuster, Rebecca M et al. (2012) Proinflammatory chemokines in the intestinal lumen contribute to intestinal dysfunction during endotoxemia. Shock 37:63-9|
|Makley, Amy T; Goodman, Michael D; Belizaire, Ritha M et al. (2012) Damage control resuscitation decreases systemic inflammation after hemorrhage. J Surg Res 175:e75-82|
|Davis, Dawn T; Johannigman, Jay A; Pritts, Timothy A (2012) New strategies for massive transfusion in the bleeding trauma patient. J Trauma Nurs 19:69-75|
|Sonnier, Dennis I; Makley, Amy T; Friend, Lou Ann W et al. (2011) Hemorrhagic shock induces a proinflammatory milieu in the gut lumen. J Surg Res 170:272-9|
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