Lipid mediators in the pathophysiology of critical illness.
Inflammatory lipid mediators are produced by the metabolism of membrane phospholipids following a number of different stimuli. These mediators lead to a variety of cellular and systemic responses which contribute to the manifestations of the systemic inflammatory response syndrome in the critically ill patient. These mediators include platelet-activating factor and the eicosanoids, including prostaglandins, thromboxanes, leukotrienes, and HETEs. This review seeks to evaluate the current role of these mediators in the pathophysiology of critical illness. We will focus on recent studies concerning the modulation of these pathways as a potential therapeutic strategy for management of these critically ill patients. This includes the gamut from nutritional strategies to alter the cellular membrane lipid composition, thereby effecting the substrate available to produce these lipid byproducts, to intracellular inhibitors to alter production of these mediators, to receptor blockage and enhanced clearance to inhibit their effects.
Bulger
E M
EM
Department of Surgery, University of Washington, Harborview Medical Center, Seattle 98104, USA.
Maier
R V
RV
D002462:Cell Membrane / Q000378:metabolism; D016638:Critical Illness; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D008055:Lipids / Q000502:physiology*; D010741:Phospholipases A / Q000096:biosynthesis / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism; D011453:Prostaglandins / Q000502:physiology*; D012128:Respiratory Distress Syndrome / Q000378:metabolism / Q000503:physiopathology; D015290:Second Messenger Systems / Q000502:physiology; D018805:Sepsis / Q000503:physiopathology; D012769:Shock / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000517:prevention & control
D018836:Inflammation Mediators; D008055:Lipids; D010743:Phospholipids; D011453:Prostaglandins; D010741:Phospholipases A