Hypertonic saline acts on septic lung remodeling through nitric oxide‐induced FAK activation pathway

Abstract

Hypertonic saline solution (HS, NaCl 7,5%) has shown to modulates immune function and decrease pulmonary injury triggered by endotoxic shock. Our objective was to investigate the effects of HS on the mechanism involved in pulmonary fibrosis, in an experimental model of endotoxemic shock. Wistar rats received lipopolysaccharide ‐ LPS (10mg/kg i.p.) and volume i.v. after 15 minutes. The animals were assigned in four groups (n=7): control group (not subjected to LPS); LPS group (injected with LPS 10mg/kg i.p); HS group (treated with hypertonic saline, 4 mL/Kg i.v. after LPS) and NS group (treated with normal saline, 34 mL/kg i.v. after LPS). At 24h after treatment, pulmonary mechanics, type I and type III collagen expression, metalloproteinase 9 expression, focal adhesion kinase (FAK) and nitric oxide synthesis were measured. NS increased pulmonary resistance and elastance, compared to other groups. HS inhibited collagen expression compared to LPS and NS groups and prevented pulmonary injury by decreased MMP9 activity in tissue. Expression of FAK was decreased in HS groups compared to LPS and NS groups. NO expression was decreased in HS group, compared to LPS and NS groups. We concluded that treatment of endotoxemic shock with HS solution act on nitric oxide‐induced FAK activation pathway, which could modulate the collagen deposition in pulmonary tissue, and consequently decrease the progression of pulmonary fibrosis