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Normal saline resuscitation induces increased sinusoidal MIP‐2 expression in early sepsis
Author(s) -
Patrick Amanda L,
FoxRobichaud Alison E
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.731.8
Subject(s) - resuscitation , saline , sepsis , medicine , chemokine , microcirculation , intravital microscopy , anesthesia , pathology , immunology , inflammation
Fluid resuscitation is an integral part of the treatment of patients with severe sepsis. Common fluids administered within the first 6 hours of diagnosis include normal saline and Ringer's lactate, however, currently there is no clear evidence that support the use of one resuscitation fluid over another. Previous work in our lab demonstrated that normal saline increases leukocyte‐endothelial cell interactions. The objective in this study was to determine the mechanisms for saline‐induced hepatic leukocyte recruitment. Sepsis was induced by cecal ligation and perforation in C57Bl/6 mice. Septic, sham‐operated or naïve mice received an IV bolus (20mL/kg) of Ringer's lactate or normal saline (0.9% NaCl). Six hours later the hepatic microcirculation was examined by confocal intravital microscopy to visualize the neutrophil chemokine macrophage inflammatory protein‐2 (MIP‐2) expression using an Alexafluor conjugated monoclonal antibody. MIP‐2 expression, as measured by mean fluorescent intensity, was significantly higher in the hepatic sinusoids of septic mice treated with normal saline compare to septic mice given Ringer's lactate. The use of normal saline as an intravenous resuscitation fluid was associated with increased chemokine expression in the both sinusoids and post‐sinusoidal venules. These data suggest that saline treatment in early sepsis augments neutrophil recruitment by increasing endothelial cell chemokine expression.