The effects of propranolol and clonidine on bone marrow expression of hematopoietic cytokines following trauma and chronic stress.
Am J Surg
; 218(5): 858-863, 2019 11.
Article
em En
| MEDLINE
| ID: mdl-30827533
ABSTRACT
BACKGROUND:
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).METHODS:
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.RESULTS:
Following LCHS, HMGB1 was decreased by propranolol (49% decrease, pâ¯=â¯0.012) and clonidine (54% decrease, pâ¯<â¯0.010). SCF was decreased following LCHS/CS, and was increased by propranolol (629% increase, pâ¯<â¯0.001) and clonidine (468% increase, pâ¯<â¯0.001). Bcl-xL was decreased following LCHS/CS, and was increased by propranolol (59% increase, pâ¯=â¯0.006) and clonidine (77% increase, pâ¯<â¯0.001).CONCLUSIONS:
Following severe trauma, propranolol and clonidine abrogate persistent injury-associated anemia by modulating bone marrow cytokines, favoring effective erythropoiesis.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Propranolol
/
Estresse Fisiológico
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Medula Óssea
/
Citocinas
/
Clonidina
/
Lesão Pulmonar
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Hematínicos
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article