title: Alert cell strategy: mechanisms of inflammatory response and organ protection.
abstract: Systemic inflammatory response syndrome (SIRS) is triggered by various factors such as surgical operation, trauma, burn injury, ischemia, pancreatitis and bacterial translocation. Sepsis is a SIRS associated with bacterial infection. SIRS and sepsis tend to trigger excessive production of inflammatory cytokines and other inflammatory molecules and induce multiple organ failure, such as acute lung injury, acute kidney injury and inflammatory cardiac injury. Epithelial and endothelial cells in some major organs express inflammatory receptors on the plasma membrane and work as alert cells for inflammation, and regulation of these alert cells could have a relieving effect on the inflammatory response. In inflammatory conditions, initial cardiac dysfunction is mediated by decreased preload and adequate infusion therapy is required. Tachyarrhythmia is a complication of inflammatory conditions and early control of the inflammatory reaction would prevent the structural remodeling that is resistant to therapies. Furthermore, there seems to be crosstalk between major organs with a central focus on the kidneys in inflammatory conditions. As an alert cell strategy, volatile anesthetics, sevoflurane and isoflurane, seem to have anti-inflammatory effects, and both experimental and clinical studies have shown the beneficial effects of these drugs in various settings of inflammatory conditions. On the other hand, in terms of intravenous anesthetics, propofol and ketamine, their current status is still controversial as there is a lack of confirmatory evidence on whether they have an organ-protective effect in inflammatory conditions. The local anesthetic lidocaine suppressed inflammatory responses upon both systemic and local administration. For the control of inflammatory conditions, anesthetic agents may be a target of drug development in accordance with other treatments and drugs.
authors.forename: Noboru
authors.initials: N
authors.lastname: Hatakeyama
authors.affiliation: Department of Emergency and Critical Care Medicine, Nagoya University Graduate School of Medicine. nmatsuda@med.nagoya-u.ac.jp.
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Matsuda
mesh_terms: D000777:Anesthetics / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000494:pharmacology; D016207:Cytokines / Q000378:metabolism; D015195:Drug Design; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D009102:Multiple Organ Failure / Q000209:etiology / Q000517:prevention & control; D018805:Sepsis / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D018746:Systemic Inflammatory Response Syndrome / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D000777:Anesthetics; D000893:Anti-Inflammatory Agents; D016207:Cytokines