Medical science monitor : international medical journal of experimental and clinical research
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Hemorrhagic shock occasionally causes a fatal outcome following an outbreak of lung dysfunction, but the precise mechanism has not been clearly elucidated. Several studies have indicated that hemorrhagic shock causes a delayed vascular inflammatory decompensation and leads to inflammation-related organ dysfunction. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta are known as major proinflammatory cytokines that play an important role in excessive autolytic inflammation, finally inducing organ dysfunctions. In this study, the role of TNF-alpha and IL-1beta on lung dysfunction following hemorrhagic shock was examined by using FR167653, a potent inhibitor of TNF-alpha and IL-1beta production that acts by suppressing p38 mitogen-activated protein kinase (MAPK). ⋯ TNF-alpha and IL-1beta play a key role in the development of inflammation-related lung dysfunction following hemorrhagic shock. Our model should be useful to explain the pathogenesis of lung dysfunction following hemorrhagic shock.
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Preoperative atrial fibrillation (AF) increases the risk of cardiac surgery and the occurrence of postoperative complications, including arrhythmias, low-output syndrome, delirium, and death. The aim was to evaluate its direct influence on prognosis of patients subjected to cardiac surgery. ⋯ Preoperative AF was an independent risk factor of postoperative delirium (OR=7.2). It was also associated with significantly worse postoperative outcome (supraventricular arrhythmia, stroke, low-output syndrome, and risk of death). These results and data from available studies suggest that preoperative AF should be considered as an important predictor of postoperative outcome. This problem should be the subject of future research to establish beneficial treatment options.