Hypertonic Saline Inhibits Leukotriene B4 And Arachidonic Acid Priming Of The Neutrophil Oxidase

Abstract

Introduction: Previous work shows that arachidonic acid (AA, and its leukotriene derivatives e.g.: LTB4) is an inflammatory mediator in post-shock mesenteric lymph (PSML), and in stored packed RBCs. AA appears to act as an agonist at LTB4 G-protein coupled receptors (GPCRs). These mediators prime neutrophils (PMNs) for an increased production of superoxide, resulting in ALI. Hypertonic Saline (HTS) have also been shown to have immunomodulatory effects such as attenuation of PMN respiratory burst via signaling GPCRs, thereby potentially attenuating ALI.