Besides a possible role of different intravascular volume status (although the comparable central venous pressures in both age groups are not suggestive of that), systemic inflammation is a possible reason for this finding: IL-1β concentrations were highest in the animal group exhibiting the strongest hemodynamic depression (old animals ventilated with the highest VT) and an increase in IL-1β blood concentrations has been shown to induce arterial hypotension and cardiac depression in both rodents and humans [34-36]. This evidence concerns the gene IL1B and hypotensive disorder.