Eicosanoids derived from cytochrome P450 pathway of arachidonic acid and inflammatory shock

Publication date: Available online 3 October 2019Source: Prostaglandins & Other Lipid MediatorsAuthor(s): Bahar Tunctan, Sefika Pinar Senol, Meryem Temiz-Resitoglu, Demet Sinem Guden, Seyhan Sahan-Firat, John R. Falck, Kafait U. MalikAbstractSepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock, the most common form of vasodilatory shock, is a subset of sepsis in which circulatory and cellular/metabolic abnormalities are severe enough to increase mortality. Inflammatory shock constitutes the hallmark of sepsis, but also a final common pathway of any form of severe long-term tissue hypoperfusion. The pathogenesis of inflammatory shock seems to be due to circulating substances released by pathogens (e.g., bacterial endotoxins) and host immuno-inflammatory responses (e.g., changes in the production of histamine, bradykinin, serotonin, nitric oxide [NO], reactive nitrogen and oxygen species, and arachidonic acid [AA]-derived eicosanoids mainly through NO synthase, cyclooxygenase, and cytochrome P450 [CYP] pathways, and proinflammatory cytokine formation). Therefore, refractory hypotension to vasoconstrictors with end-organ hypoperfusion is a life threatening feature of inflammatory shock. This review summarizes the current knowledge regarding the role of eicosanoids derived from CYP pathway of AA in animal models of inflammatory shock syndromes with an emphasis on septic shock in addition to potential therapeutic strategi...
Source: Prostaglandins and Other Lipid Mediators - Category: Lipidology Source Type: research