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The effects of propranolol and clonidine on bone marrow expression of hematopoietic cytokines following trauma and chronic stress

Attenuating 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 gro...

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Published in:The American journal of surgery 2019-11, Vol.218 (5), p.858-863
Main Authors: Loftus, Tyler J., Miller, Elizabeth S., Millar, Jessica K., Kannan, Kolenkode B., Alamo, Ines G., Efron, Philip A., Mohr, Alicia M.
Format: Article
Language:English
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Summary:Attenuating 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). Male 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. Following LCHS, HMGB1 was decreased by propranolol (49% decrease, p = 0.012) and clonidine (54% decrease, p 
ISSN:0002-9610
1879-1883
DOI:10.1016/j.amjsurg.2019.02.023