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.

Public Health Relevance

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.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08GM088589-03
Application #
8287132
Study Section
Surgery, Anesthesiology and Trauma Study Section (SAT)
Program Officer
Somers, Scott D
Project Start
2010-07-01
Project End
2013-06-30
Budget Start
2012-07-01
Budget End
2013-06-30
Support Year
3
Fiscal Year
2012
Total Cost
$132,327
Indirect Cost
$9,802
Name
University of Cincinnati
Department
Surgery
Type
Schools of Medicine
DUNS #
041064767
City
Cincinnati
State
OH
Country
United States
Zip Code
45221
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
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
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
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