• Tyler J Loftus, Elizabeth S Miller, Jessica K Millar, Kolenkode B Kannan, Ines G Alamo, Philip A Efron, and Alicia M Mohr.
• University of Florida, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, USA. Electronic address: Tyler.Loftus@surgery.ufl.edu.
• Am. J. Surg. 2019 Nov 1; 218 (5): 858-863.

BackgroundAttenuating post-injury neuroendocrine stress abrogates persistent injury-associated anemia. Our objective was to examine the mechanisms by which propranolol and clonidine modulate this process. We hypothesized that propranolol and clonidine would decrease bone marrow expression of high-mobility group box-1 (HMGB1) and increase expression of stem cell factor (SCF) and B-cell lymphoma-extra large (Bcl-xL).MethodsMale Sprague-Dawley rats were allocated to naïve control, lung contusion followed by hemorrhagic shock (LCHS), or LCHS plus daily chronic restraint stress (LCHS/CS) ±propranolol, ±clonidine. Day seven bone marrow expression of HMGB1, SCF, and Bcl-xL was assessed by polymerase chain reaction.ResultsFollowing LCHS, HMGB1 was decreased by propranolol (49% decrease, p = 0.012) and clonidine (54% decrease, p < 0.010). SCF was decreased following LCHS/CS, and was increased by propranolol (629% increase, p < 0.001) and clonidine (468% increase, p < 0.001). Bcl-xL was decreased following LCHS/CS, and was increased by propranolol (59% increase, p = 0.006) and clonidine (77% increase, p < 0.001).ConclusionsFollowing severe trauma, propranolol and clonidine abrogate persistent injury-associated anemia by modulating bone marrow cytokines, favoring effective erythropoiesis.Copyright © 2019 Elsevier Inc. All rights reserved.

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