OXIDATIVE STRESS IN THE DEVELOPMENT OF HUMAN ISCHEMIC HEPATITIS DURING CIRCULATORY SHOCK

An increasing number of studies support the involvement of free radica l-mediated oxidative reactions in the pathogenesis of tissue injury fo llowing ischemia reperfusion. In particular, a condition of oxidative stress is evident in patients with circulatory shock, a disease proces s often complicated by progressive organ failure sustained by inflamma tory reactions. In all shock patients without signs of organ failure, a consistent increase of intermediate and final products of Lipid pero xidation (lipid peroxides and aldehydes respectively) was observed. Im pairment of the redox equilibrium in the tissues of these patients was confirmed by a significant reduction of glutathione and vitamin E hem atic concentrations. Moreover, a selective increase of plasma aldehyde -protein adducts, actual proof of oxidative damage of macromolecules, is only present in the shock patients who, in addition, show hepatic c ytolysis (ischemic hepatitis) as estimated by plasma levels of LDH(5) isoenzyme. Aldehyde adducts well mark the progression of the disease t owards multiple organ failure. Finally, the good statistical correlati on between aldehyde-modified proteins and LDH(5), as well as their dis tinct behaviour in control and ischemic hepatitis, support the involve ment of oxidative damage in the expression and worsening of circulator y shock.