The effects of selective beta-adrenergic blockade on bone marrow dysfunction following severe trauma and chronic stress.

INTRODUCTION: Propranolol has been shown to improve erythroid progenitor cell growth and anemia following trauma and this study sought to investigate the mechanisms involved by evaluating the effects of selective beta blockade. METHODS: Male Sprague-Dawley rats were subjected to lung contusion, hemorrhagic shock and chronic stress (LCHS/CS) ± daily selective beta-1, beta-2, or beta-3 blockade (B1B, B2B, B3B). Bone marrow cellularity and growth of erythroid progenitor colonies, hemoglobin, plasma granulocyte colony-stimulating factor (G-CSF), hematopoietic progenitor cell mobilization, and daily weight were assessed. RESULTS: Selective beta-2 and beta-3 blockade improved bone marrow cellularity, erythroid progenitor colony growth and hemoglobin levels, while decreasing plasma G-CSF, progenitor cell mobilization and weight loss following LCHS/CS. CONCLUSIONS: Attenuating the neuroendocrine stress response with the use of selective beta-2 and 3 adrenergic blockade may be an alternative to improve bone marrow erythroid function following trauma.

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. Liver expression of IL-6 and TNF-α were assessed with real time PCR. RESULTS: Chronic stress at 7 and 14 days sequentially increased plasma acute phase reactants (NE, IL-6, TNF-α, and CRP), liver IL-6 expression, hematopoietic progenitor cell mobilization, and decreased erythroid progenitor colony growth. Weight gain was reduced by chronic stress compared to each models' naïve counterpart. CONCLUSIONS: Combining this model with trauma and sepsis models will allow evaluation of the contribution of persistent inflammation in disease progression and outcomes.