Mediators play a key role in the development of systemic inflammatory
response syndrome (SIRS), multiple organ dysfunction syndrome, and mul
tiple organ failure of vital organs. In this short review we update ou
r knowledge on these mediator network. First, we summarize the stimuli
that occur during severe trauma (intraoperative stress), including po
lymorphonuclear neutrophil-derived tissue-damaging substances, complem
ent activation products, and adherence molecules such as selectins. Th
e gut in shock is discussed as an important intermediate step in the t
ransition from noninfectious to infectious SIRS. Second, we describe t
he mediators, including cytokines, nitric oxide, phospholipase A(2), p
latelet-activating factor, and procoagulatory substances, that are rel
eased during sepsis. The release of mediators depends primarily on the
severity of the trauma, shock, or sepsis and secondarily on the activ
ation of the various cascades of mediators during posttraumatic/postop
erative complications. The mediators are thus of decisive importance r
egarding the intensity of organ damage and the outcome.