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 oxida se after ischemia/reperfusion, toxic oxygen species from phagocytes th at accumulate in both intra- and extravascular tissue spaces are of ce ntral importance. A critical event is the contact (adhesion) of leukoc ytes to endothelial cells, which consequently are the targets for leuk ocyte products. Damage of membranes by lipid peroxidation and by expos ure to mediators such as platelet activating factor (PAF), leukotriene s and proteases, leads to increased permeability, tissue oedema and or gan dysfunction. Thus antioxidants and other agents that control phago cyte function are likely to contribute to the protection of the permea bility barrier in shock states.