THE DETRIMENTAL EFFECTS OF cardiopulmonary
bypass (CPB) on inflammation pathways have been
studied extensively, and a central role of the post-CPB
inflammatory response in the pathophysiology of endothelial
dysfunction has been emphasized repeatedly.
1–3 Several studies were performed in patients undergoing CPB to assess its
pathophysiologic effects on endothelial function, but all inves-tigated the cellular and molecular pathways involved, without a systematic detection of its functional correlates