2013
DOI: 10.1016/j.cppeds.2013.10.001
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Definitions and Pathophysiology of Sepsis

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Cited by 82 publications
(73 citation statements)
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“…The inflammatory response in sepsis is characterized by excess production of pro-inflammatory cytokines, primarily TNF-α, IL-1β and IL-6, such that production of anti-inflammatory mediators is not adequately counterbalanced, mainly in the initial phase (Sagy et al, 2013). This imbalance in cytokine production causes endothelial lesions, pulmonary edema and hemorrhage, and may evolve to terminal complications associated with sepsis (MODS) (Zhou et al, 2015).…”
Section: Discussionmentioning
confidence: 99%
“…The inflammatory response in sepsis is characterized by excess production of pro-inflammatory cytokines, primarily TNF-α, IL-1β and IL-6, such that production of anti-inflammatory mediators is not adequately counterbalanced, mainly in the initial phase (Sagy et al, 2013). This imbalance in cytokine production causes endothelial lesions, pulmonary edema and hemorrhage, and may evolve to terminal complications associated with sepsis (MODS) (Zhou et al, 2015).…”
Section: Discussionmentioning
confidence: 99%
“…Compromised cardiac contractile function has been reported in patients with sepsis [1]. LPS, the major component of the bacterial outer membrane, plays an important role in the pathogenesis of cardiac anomalies in sepsis [13,14].…”
Section: Furthermore Esmolol Infusion Inhibited the Lps-enhanced Actmentioning
confidence: 99%
“…Sepsis, as a systemic response to infection, results in significant physiologic derangements, leads to multiple organ dysfunction and death, and places a substantial financial burden on the health care system [1]. Lipopolysaccharide (LPS) as an endotoxin, one of the important inflammatory mediators in major surgical injury, is a component of the outer membrane of most gram-negative bacteria, and plays a central role in sepsis [2].…”
Section: Introductionmentioning
confidence: 99%
“…Toksinler dolaşıma karıştığı zaman makrofajları etkinleştirerek MAPK ve NF-κB aracılıklı interlökin (IL)-1, IL-6, IL-8 ve tümor nekrozlaştırıcı faktör-α (TNF-α) gibi birçok enflamatuvar sitokin salıverilmesine yol açmaktadır. Ayrıca ekzotoksinler; T-lenfositleri gibi efektör hücreleri etkinleştirerek indükle-nebilir nitrik oksit sentaz (iNOS) uyarılmasıyla nitrik oksit (NO) oluşumuna neden olan IL-2 ve IFN-γ gibi proenflamatuvar mediyatörlerin üretimini artırmaktadır (25)(26)(27). Bunun dışında septik şokta platelet aktive edici faktör (plateletactivating factor; PAF), tromboksan (Tx) A 2 , prostaglandin (PG) E 2 , lökotrienler, makrofaj enflamatuvar protein-1, siklooksijenaz (COX)-2, haberci ribonükleik asit (messenger ribonucleic acid; mRNA) ve ET-1 düzeylerinin artmış olduğu bulunmuştur (27)(28)(29).…”
Section: Toll-interleukin 1 Receptor Domain-containing Adapter-induciunclassified