Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiopulmonary bypass (CPB) is known to cause a systemic inflammatory response. Inflammation includes several cascade activations: complement, cytokine, and coagulation. The early phase is triggered by blood contact with the synthetic bypass circuit and the late phase by ischemia-reperfusion and endotoxemia. Systemic inflammatory response syndrome (SIRS) is constant following cardiac surgery; however, a compensatory anti-inflammatory response is also constant and the clinical manifestations (varying from uncomplicated SIRS to shock and multiple organ dysfunction) depend on the balance between the two responses. When overexpressed, the inflammatory response may significantly increase a patient's risk. Minimization of systemic inflammation is a major concern and several strategies aiming to inhibit the inflammatory response are described. None of them is satisfactory, but the "control" of the inflammatory response extent is likely to require a multimodal approach. This review aims to describe the strategies proposed to reduce CPB-related systemic inflammation.
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PMID:Minimizing systemic inflammation during cardiopulmonary bypass in the pediatric population. 2439 66

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.
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PMID:Alert cell strategy: mechanisms of inflammatory response and organ protection. 2522 71