Involvement of oxygen radicals in shock related cell injury.

Shock-related organ failure evolves from a variety of starting points--ischemia, reperfusion, non-bacterial or bacterial inflammation--several mechanisms are involved. In addition to the effects of xanthine oxidase after ischemia/reperfusion, toxic oxygen species from phagocytes that accumulate in both intra- and extravascular tissue spaces are of central importance. A critical event is the contact (adhesion) of leukocytes to endothelial cells, which consequently are the targets for leukocyte products. Damage of membranes by lipid peroxidation and by exposure to mediators such as platelet activating factor (PAF), leukotrienes and proteases, leads to increased permeability, tissue oedema and organ dysfunction. Thus antioxidants and other agents that control phagocyte function are likely to contribute to the protection of the permeability barrier in shock states.