Nihon Geka Gakkai zasshi
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Reperfusion injury is recognized as a syndrome which impairs an ischemic organ as well as remote organs throughout the entire body. Previous research has revealed that the various inflammatory mediators, such as cytokines, platelet-activating factors, and free radicals, are involved and interact with each other in reperfusion injury. More recently, it has been demonstrated that neutrophils play an important role in the development of reperfusion injury. ⋯ The same systemic reaction is also observed in multiple organ failure (MOF) or systemic inflammatory response syndrome (SIRS), where organ failure is a major determinant factor for the prognosis of patients. Regarding the treatment of organ failure due to reperfusion injury, several approaches using monoclonal antibody of adhesion molecules or receptor antagonist for cytokines have been introduced. Despite the current accumulation of knowledge, however, prevention is still the regimen for reperfusion injury and concomitant organ failure.
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Multiple organ failure (MOF) is a critical condition developing in patients with overwhelming bodily injury resulting from major surgical insult, severe trauma, extensive burns, acute pancreatitis, and sepsis. It has recently become evident that the host response to such injury is the main pathogenetic factor contributing to the development of MOF. The proinflammatory cytokines tumor necrosis factor (TNF) and interleukin (IL)-1 are known to play a pivotal role in the pathogenetic mechanisms of MOF. ⋯ The resultant systemic inflammation may develop into MOF mainly through neutrophil-endothelial cell interaction when the primary injury is overwhelming or a second inflammatory insult such as sepsis triggers an exacerbated inflammation. It has recently been confirmed that the transcription factor NF-kappaB is involved in the up-regulation of a variety of proinflammatory genes and that cell-mediated immunity is down-regulated in the event of major bodily injury through a shift in the balance between T helper 1 (Th1) and Th2 cytokine response patterns. The molecular immunological mechanisms by which these factors participate in the development of MOF should be characterized.