Sepsis eicosanoids

Nearly all cells express kinin receptors that mediate the activities of both bradykinin and kallidin. The activation of these G-protein coupled receptors causes relaxation of venular smooth muscle and hypotension, increased vascular permeability, contraction of smooth muscle of the gut and airway leading to increased airway resistance, stimulation of sensory neurons, alteration of ion secretion of epithelial cells, production of nitric oxide, release of cytokines from leukocytes, and the production of eicosanoids from various cell types [11,12]. Because of this broad spectrum of activity, kinins have been implicated as an important mediator in many pathophysiologies including pain, sepsis, asthma, rheumatoid arthritis, pancreatitis, and a wide variety of other inflammatory diseases. Moreover, a recent report demonstrated that bradykinin B2 receptors on the surface of human fibroblasts were upregulated three-fold beyond normal in patients with Alzheimer s disease, implicating bradykinin as a participant in the peripheral inflammatory processes associated with that disease [13]. 

The effect of glucan on survival time and eicosanoid synthesis in the rat faecal peritonitis (LDioq) model has also been assessed . A high dose of glucan decreased survival time from 11.5 0.4 h to 7.3 0.5 h during sepsis... 

Meaningful interpretation of eicosanoid levels in plasma or pulmonary oedema fluid during clinical sepsis or ARDS is complicated by the large number of uncontrolled variables compared with experimental sepsis or models of acute lung injury. These include diverse etiological factors precipitating sepsis and ARDS, variation in the stage of severity of these inflammatory conditions... 

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