Aims: In this project we want to further elucidate the role of NO and of alternative pathways of
vasodilation in inflammatory shock. More in particular we want to
1/ identify the factors determining whether NO release will have hemodynamic effects or not
2/ to determine which NO independent factors are relevant in inflammatory shock
3/ to explore the role of the downstream target of NO, soluble guanylate cyclase (sGC)
4/ to determine the relation between (inhibition) of vasorelaxation and tissue perfusion