Michael A Flierl, Daniel Rittirsch, Sebastian Weckbach, Markus Huber-Lang, Kyros Ipaktchi, Peter A Ward and Philip F Stahel
Annals of Intensive Care 2011, 1:53 doi:10.1186/2110-5820-1-53
Published: 30 December 2011
Sepsis continues to be a poorly understood syndrome with a high mortality rate. While we are beginning to decipher the intricate interplay of the inflammatory response during sepsis, the precise regulation of the hypothalamic-pituitary-adrenal (HPA) axis and its impact on electrolyte homeostasis during sepsis remains incompletely understood.
Sepsis was induced in adult male Sprague-Dawley rats by cecal ligation and puncture (CLP). Plasma samples were obtained as a function of time (6-48 hrs) after CLP and compared to healthy animals (neg ctrl). Samples were analyzed for adrenocorticotropin (ACTH), corticosterone, and aldosterone levels as well as concentrations of sodium (Na+), potassium (K+), chloride (Cl-) and magnesium (Mg2+).
ACTH levels were found to be significantly reduced 6-24 hrs after CLP in comparison to baseline levels and displayed gradual recovery during the later course (24-48 hrs) of sepsis. Plasma corticosterone concentrations exhibited a bell-shaped response, peaking between 6 and 12 hrs followed by rapid decline and concentrations below negative control levels 48 hrs after injury. Aldosterone levels in septic animals were continuously elevated between 6 and 48 hrs. While plasma Na+ levels were found to be persistently elevated following CLP, levels of K+, Cl- and Mg2+ were significantly reduced as a function of time and gradually recovered during the later course of sepsis.
CLP-induced sepsis resulted in dynamic changes of ACTH, corticosterone and aldosterone levels. In addition, electrolyte levels showed significant disturbances following CLP. These electrolyte perturbations might be evoked by a downstream effect or a dysfunctional HPA-axis response during sepsis and contribute to severe complications during sepsis.
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