As potent inflammatory mediators, IL-6 and TNF-α stimulate the expression of endothelial adhesion molecules, thereby promoting leukocyte adhesion and transmigration, augmenting the release of inflammatory mediators into tissues, and driving systemic inflammation in the early post-resuscitation period; these processes further aggravate myocardial depression, endothelial dysfunction, and microcirculatory failure.34 This evidence concerns the gene IL6 and endothelial dysfunction.