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About the Authors:
Morten Zaar
Contributed equally to this work with: Morten Zaar, Chriselda G. Fedyk
* E-mail: [email protected]
Affiliation: University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America
Chriselda G. Fedyk
Contributed equally to this work with: Morten Zaar, Chriselda G. Fedyk
Affiliation: United States Army Institute of Surgical Research, Fort Sam Houston, Texas, United States of America
Heather F. Pidcoke
Affiliation: United States Army Institute of Surgical Research, Fort Sam Houston, Texas, United States of America
Michael R. Scherer
Affiliation: United States Army Institute of Surgical Research, Fort Sam Houston, Texas, United States of America
Kathy L. Ryan
Affiliation: United States Army Institute of Surgical Research, Fort Sam Houston, Texas, United States of America
Caroline A. Rickards
Affiliation: University of North Texas Health Science Center Fort Worth, Fort Worth, Texas, United States of America
Carmen Hinojosa-Laborde
Affiliation: United States Army Institute of Surgical Research, Fort Sam Houston, Texas, United States of America
Victor A. Convertino
Affiliation: United States Army Institute of Surgical Research, Fort Sam Houston, Texas, United States of America
Andrew P. Cap
Affiliation: United States Army Institute of Surgical Research, Fort Sam Houston, Texas, United States of America
Introduction
Central hypovolemia elevates hemostatic activity whether it is provoked by controlled bleeding [1], [2], simulated bleeding by lower body negative pressure (LBNP) [3], [4], or orthostatic stress [5]. The hemostatic system is composed of several components that create a dynamic balance between coagulation and fibrinolysis, to reduce bleeding after injury while maintaining or restoring vascular patency. Both coagulation and fibrinolytic activities are regulated by components released from the vasculature (e.g., von Willebrand factor (vWF) and tissue-type plasminogen activator (t-PA)), and are likely regulated in part by increased sympathetic activity resulting from central hypovolemia [6], [7]. However, there is also a cell-based component of elevated hemostatic activity in which coagulation is regulated by the surface of activated platelets [8]. There are a number of pathways, including stimulation by catecholamines, which result in platelet activation. Cross-talk between these pathways increases the complexity of analyzing the platelet contribution to coagulation. Activation of platelets results in conversion of glycoprotein IIb/IIIa (GPIIb/IIIa) into its active form, which is central for platelet aggregation [9]. Thus, activated platelets are essential for hemostasis...