ORIGINAL ARTICLESExamining platelet–fibrin interactions during traumatic shock in a swine model using platelet contractile force and clot elastic modulusWhite, Nathan J.a,b; Martin, Erika J.c; Brophy, Donald F.a,c; Ward, Kevin R.a,bAuthor Information aReanimation Engineering Science Center bDepartment of Emergency Medicine cDepartment of Pharmacy, Virginia Commonwealth University, Richmond, Virginia, USA Correspondence to Nathan J. White, MD, Division of Emergency Medicine, Harborview Medical Center, Box 359702, 325 9th Avenue, Seattle, WA 98104, USATel: +1 206 744 8465; e-mail: firstname.lastname@example.org Received 17 September, 2010 Revised 25 January, 2011 Accepted 5 February, 2011 These data were presented in preliminary form at the 2008 Annual meeting of the Society for Academic Emergency Medicine, Washington, District of Columbia, USA and at the 2009 22nd Congress of the International Society on Thrombosis and Haemostasis Boston, Massachusetts, USA. Blood Coagulation & Fibrinolysis: July 2011 - Volume 22 - Issue 5 - p 379-387 doi: 10.1097/MBC.0b013e3283456c68 Buy Metrics Abstract A significant proportion of severely injured patients develop early coagulopathy, characterized by abnormal clot formation, which impairs resuscitation and increases mortality. We have previously demonstrated an isolated decrease in clot strength by thrombelastography in a swine model of nonresuscitated traumatic shock. In order to more closely examine platelet–fibrin interactions in this setting, we define the observed decrease in clot strength in terms of platelet-induced clot contraction and clot elastic modulus using the Hemostasis Analysis System (HAS) (Hemodyne Inc., Richmond, Virginia, USA). Whole blood was sampled for HAS measurements, metabolic measurements, cell counts, and fibrinogen concentration at baseline prior to injury and again at a predetermined level of traumatic shock defined by oxygen debt. Male swine (N = 17) received femur fracture and controlled arterial hemorrhage to achieve an oxygen debt of 80 ml/kg. Platelet counts were unchanged, but fibrinogen concentration was reduced significantly during shock (167.6 vs. 66.7 mg/dl, P = 0.0007). Platelet contractile force generated during clot formation did not change during shock (11.7 vs. 10.4 kdynes, P = 0.41), but clot elastic modulus was dynamically altered, resulting in a lower final value (22.9 vs. 17.3 kdynes/cm2, P < 0.0001). In this model of traumatic shock, platelet function was preserved, whereas terminal clot elastic modulus was reduced during shock in a manner most consistent with early changes in the mechanical properties of the developing fibrin fiber network. © 2011 Lippincott Williams & Wilkins, Inc.