Macrophage Migration Inhibitory Factor (MIF)- Cardiac Surgery

Status Completed

Clinical Trial Summary

It has been repeatedly demonstrated that cardiac surgery with the use of extracorporeal circulation elicits a systemic inflammatory response and provokes ischemia-reperfusion related oxidative stress which could further lead to the development of organ failure in critically ill patients. Perioperative levels of macrophage migration inhibitory factor (MIF) and other inflammatory mediators could be involved in adverse outcomes in cardiac surgery.

Clinical Trial Description

The trace element selenium (Se) serves as an essential co-factor for the antioxidant enzymes Thioredoxin - reductase (TRR) and many other antioxidant enzymes, which protect tissues from oxidative stress. In septic patients it has previously been shown that thioredoxin, a TRR regulated Redox Enzyme, has the ability to suppress the synthesis of MIF.

Aim of the present study is therefore to investigate the relation between perioperative selenium decrease and the reduction of TRR activity with a possible release of MIF during the inflammatory response after cardiac surgery. ;

Study Design

Observational Model: Cohort, Time Perspective: Prospective

Related Conditions & MeSH terms

Heart Surgery

Clinical Trial Details

NCT number	NCT01267721
Study type	Observational
Source	RWTH Aachen University
Contact
Status	Completed
Phase	N/A
Start date	January 2011

View Details

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