Inflammatory Response to cardiac surgery

A) Disturbances of the anti-oxidative capacity during/following cardiac surgery

Oxidative stress is increasingly being recognized as a major factor contributing to the development of organ failure in critically ill patients. The generation of cytotoxic reactive oxygen species (ROS) results in cellular injury and activates inflammatory pathways by stimulating the expression of proinflammatory transcription factors.

In mammalians, a sophisticated endogenous defense system protects tissues from oxidative stress. As an example, several enzymes such as catalase and glutathione peroxidase neutralize ROS. For these antioxidant (AOX) enzymes, the trace elements selenium (Se), zinc (Zn) and copper (Cu) serve as essential co-factors. Particular interest has been developed for Se as this semi-metal is involved in multiple steps of intracellular antioxidant defense mechanisms. An insufficient endogenous AOX capacity has been repeatedly observed in critically ill patients with a systemic inflammatory response and/or multiorgan dysfunction and shown to be associated with the severity of illness and with mortality.

It is well-known that cardiac surgery with the use of extracorporeal circulation may elicit a systemic inflammatory response and provoke ischemia-reperfusion related oxidative stress with the release of ROS. However, the pathophysiological role of AOX trace elements in the development of multiorgan injury following cardiac surgery is still only poorly understood.

B) Clinical validation of biochemical markers occurring early during the inflammatory response to cardiac surgery