Poly(ADP-ribose) polymerase activation and the pathogenesis of circulatory shock

Various forms of circulatory shock are associated with a reduced responsiveness of arteries and veins to exogenous or endogenous vasoconstrictor agents (vascular hyporeactivity), myocardial dysfunction, and disrupted intracellular energetic processes, culminating in multiple organ failure and death. Some of these alterations previously have been suggested to be related to nitric oxide (NO) overproduction, due to the activation of the endothelial isoform of NO synthase (ecNOS) in the early stage and expression of a distinct inducible isoform of NOS (iNOS) in the late stage. ^1-3.