“…The same lack of significant differences was reported between sedation with propofol and dexmedetomidine in ICUs [92]. What is interesting is the fact that these effects are not mediated in humans by GABA A receptors, which are not elicited on neutrophils' surfaces but via other mechanisms, like the inhibition of ROS production, p44/42 mitogen-activated protein kinase phosphorylation, and mitochondrial membrane potential [81,83,93,94]. Since most of these studies have been performed in animals, there is a lack of human studies where confounding factors may interfere, especially studies in critically ill patients, so prospective RCTs in critically ill patients for the potential effects of propofol sedation are mandatory.…”