The currently available data on the pathogenesis of a systemic inflammatory reaction (SIR) are reviewed in terms of dys-regulation of membrane-cytoskeletal interactions, cellular adhesion, membrane particle release, and development of endothelial dysfunction as a key factor in the genesis of SIR. Key words: systemic inflammatory reaction, membrane particles, blebbing, selectines, cytokines.

The present views of the pathogenesis of neuronal dysfunction in critical conditions are analyzed, by taking into account of impairments of cellular NAD+ metabolism, the activity of NAD+-converting enzymes, including ADP-ribosyl cyclase/CD38, the possibilities of developing new neuroprotective strategies. Key words: neuronal dysfunction, ADP-rybosyl cyclase/CD38, NAD+, critical condition.