Chronic stress induces persistent low-grade inflammation.

Introduction: This study sought to determine if the systemic cytokine profile of rodents subjected to chronic restraint stress leads to persistent low-grade inflammation.

Methods: Male Sprague-Dawley rats were subjected to restraint stress for a total of seven or fourteen days. Urine norepinephrine (NE), plasma interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP) were assessed with ELISA.

Systemic Regulation of Bone Marrow Stromal Cytokines After Severe Trauma.

Background: Traumatic injury generates a prolonged hypercatecholamine state that is associated with reduced growth of bone marrow erythroid progenitors mediated by the bone marrow stroma. The bone marrow stroma is made up of many cells including fibroblasts, which respond to inflammatory stimuli and alter the cytokine profile. We hypothesized that trauma plasma would increase bone marrow stromal fibroblast expression of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF), erythropoietin (EPO), stem cell factor (SCF), and activation of nuclear factor kappa-light-chain-enhancer of activated B cells and correlate with injury severity and anemia.

The Postinjury Inflammatory State and the Bone Marrow Response to Anemia.

Rationale: The pathophysiology of persistent injury-associated anemia is incompletely understood, and human data are sparse.

Objectives: To characterize persistent injury-associated anemia among critically ill trauma patients with the hypothesis that severe trauma would be associated with neuroendocrine activation, erythropoietin dysfunction, iron dysregulation, and decreased erythropoiesis.

Methods: A translational prospective observational cohort study comparing severely injured, blunt trauma patients who had operative fixation of a hip or femur fracture (n = 17) with elective hip repair patients (n = 22).

Persistent injury-associated anemia and aging: Novel insights.

Background: Hypercatecholaminemia and bone marrow dysfunction have been implicated in the pathophysiology of persistent injury-associated anemia. The elderly may be more vulnerable to bone marrow dysfunction due to high basal and peak catecholamine levels and impaired hematopoietic progenitor growth. We hypothesized that aging would adversely affect persistent injury-associated anemia.

Persistent injury-associated anemia in aged rats.

Background: Hypercatecholaminemia and bone marrow dysfunction have been implicated in the pathophysiology of persistent-injury associated anemia. The elderly may be vulnerable to this phenomenon due to high basal and peak catecholamine levels, impaired erythroid progenitor growth, and baseline anemia. We hypothesized that aged F344-BN rats subjected to severe trauma and chronic stress would have persistent injury-associated anemia.

Clonidine restores vascular endothelial growth factor expression and improves tissue repair following severe trauma.

Background: We hypothesized that clonidine and propranolol would increase VEGF and VEGF-receptor expression and promote lung healing following severe trauma and chronic stress.

Methods: Sprague-Dawley rats were subjected to lung contusion (LC), lung contusion/hemorrhagic shock (LCHS), or lung contusion/hemorrhagic shock/daily restraint stress (LCHS/CS). Clonidine and propranolol were administered daily.