Although the consequences of trauma or infection are normally controlled at the site of injury, loss of local control may lead to a whole body response, which has been identified clinically as the systemic inflammatory response syndrome (SIRS). If this systemic inflammatory process involves whole body infection, the condition is termed sepsis. In its worst case, SIRS results in multiple organ dysfunction occurring in approximately 30 % of septic patients, in 24 % of patients suffering from pancreatitis, in over 30 % of trauma and in 40 % of burn patients (Beal & Cerra, 1994; Davies & Hagen, 1997).Liver injury and dysfunction occurring during SIRS has often been overshadowed by concerns regarding cardiac, renal and respiratory function. The fact that liver dysfunction plays a central role in remote injury during SIRS has been supported by studies identifying liver dysfunction as one of the major factors contributing to the mortality of surgical patients suffering from multiple organ dysfunction following infrarenal aortic reconstruction (Huber et al. 1995;Maziak et al. 1998). Currently, pharmacologic protocols and mechanical devices are available to support most vital organ functions but none exists for the liver. The role of haem oxygenase (HO) in the hepatic accumulation of leukocytes in mice during the initiation of remote organ injury following normotensive limb ischaemia-reperfusion (I-R) was investigated. Remote organ injury was initiated by 1 h bilateral hindlimb ischaemia followed by either 1 or 1.5 h reperfusion (I-R) in male C57BL/6 mice. Mice were randomly assigned to either sham (no I-R, n = 4), I-R (n = 4 for both time points), I-R plus chromium mesoporphyrin (CrMP, n = 4) to inhibit HO or I-R plus haemin (n = 4) to increase HO. Leukocyte accumulation and leukocyte-endothelial interaction were directly measured using fluorescence intravital microscopy. Leukocytes were labelled via an injection of rhodamine 6G. In sinusoids the total number and the number of stationary leukocytes were assessed. In postsinusoidal venules the number of adherent and rolling leukocytes and the velocities of both red blood cells and leukocytes were measured. The total number of leukocytes increased in sinusoids of I-R mice reaching a plateau within 1 h compared with sham animals, while the number of stationary leukocytes progressively increased over the entire study period. Stationary leukocytes in sinusoids increased after 1 and 1.5 h of I-R following CrMP, while they were significantly reduced following haemin treatment compared to animals treated with I-R only. In postsinusoidal venules a progressive increase in adherent leukocytes also occurred. As observed in sinusoids, CrMP significantly increased, while haemin significantly reduced leukocyte adhesion. The number of rolling leukocytes increased after CrMP in both I-R groups (1 and 1.5 h). The velocities of rolling leukocytes declined following 1.5 h of I-R compared with sham. Haemin treatment of 1.5 h I-R animals restored the velocities back to sham levels. The calcu...

The data suggest that non-surviving patients have higher PCT and IL-10 values. Only APACHE III score and PCT plasma levels correlated with a poor outcome. Therefore, routine measurements of plasma PCT concentrations might be helpful to improve the mortality risk prediction in patients with severe sepsis.

Exposure of human erythrocytes and human venous vascular endothelial cells to an inflammatory stimulus such as endotoxin promotes a dose-dependent adhesion of erythrocytes to endothelium in a dynamic environment. These adhesive erythrocyte-endothelium interactions can be produced by exposure of either red blood cells or endothelial cells to endotoxin, with a higher degree of adhesion after activation of the endothelial cell component.