Oxidative Stress and Cardiovascular Dysfunction in Sepsis

A state of severe oxidative stress and cardiovascular dysfunction are both associated with the dysregulated immuno-inflammatory response encountered in sepsis. The hemodynamic changes seen are typically a reduction in vascular tone and myocardial depression, accompanied by a preserved or increased cardiac output. Inflammatory mediators (including cytokines, endothelial-derived factors, and reactive oxygen species), regulated by nuclear factor kappa B, appear to have an integral role in mediating this cardiovascular dysfunction. This review gives a background to the oxidative stress encountered in sepsis, together with an overview of the proposed mechanisms underlying the cardiovascular dysfunction in sepsis and the role which reactive oxygen species and oxidative stress appear to have in its pathogenesis. The results of endogenous antioxidant repletion and synthetic antioxidant administration in sepsis and their effects on the cardiovascular dysfunction seen are reviewed. The role of more direct superoxide anion inhibition is also highlighted.