Recombinant Human Superoxide Dismutase (rhSOD) and Vascular Reactivity
Status:
Completed
Trial end date:
1969-12-31
Target enrollment:
Participant gender:
Summary
Inflammation is characterised by an increased risk for cardiovascular events. Dysfunction of
the vascular endothelium caused by oxidative stress might provide a mechanistic link. In
acute and chronic inflammation, oxidative stress occurs when the production of reactive
oxygen species [ROS] (including superoxide anions [O2-]) exceeds the capacity of the
endogenous antioxidant defense systems, resulting in ROS-mediated damage. Recombinant human
superoxide dismutase (rhSOD) has shown potent antioxidant properties in in-vitro and animal
studies and has been tested in phase I clinical trials in humans. rhSOD could offer a
therapeutic option for vascular dysfunction in diseases associated with increased oxidative
stress. The investigators, therefore, want to test if the hyporesponsiveness to vasoactive
drugs (norepinephrine, acetylcholine and glyceroltrinitrate) during acute inflammation by
low-dose lipopolysaccharide (LPS) is due to the increased production of superoxide anions,
which could be scavanged by the radical scavenger rhSOD.