Septicemia and septic shock are dramatic clinical syndromes which result from acute invasion of the bloodstream by certain microorganisms or their toxic products. The clinical manifestations of septicemia and septic shock are the result of an interplay between microbial products and host mediator systems. Sepsis provokes a neuroendocrine and inflammatory response to promote survival. A variety of host mediators have been implicated in the pathogenesis of septic shock including active metabolites of the complement, kinin, and coagulation systems as well as factors released from stimulated cells, particularly, the cytokines. From the standpoint of vascular perfusion and organ function a vicious circle is established that results in altered blood flow in the microcirculation and progressive injury to the capillary endothelium and tissue. Now, all of the cytokines are not identified thus far, TNFa appears to be the most potent mediator the pathophsiology of the sepsis syndrome. In addition, other many inflammatory mediators have been identified as inflammatoy factors in sepsis. It is also likely that in the near future we will be able to take advantage of the recent developments in molecular biology and a better understanding of the pathogenesis of the septic process. [Journal of Turgut Ozal Medical Center 1996;3(4):374-381]
Key Words: Sepsis, inflammatory mediators, cytokines, pathogenesis
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