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Interact CardioVasc Thorac Surg 2006;5:531-535. doi:10.1510/icvts.2006.130765
© 2006 European Association of Cardio-Thoracic Surgery
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Work in progress report - Cardiopulmonary bypass

Impact of antioxidative treatment on nuclear factor kappa-B regulation during myocardial ischemia–reperfusion

Uwe M. Fischera,*, Albert Antonyanb, Wilhelm Blochc and Uwe Mehlhorna

a Department of Cardiothoracic Surgery, University of Cologne, Joseph-Stelzmann-Str. 9, 50924 Cologne, Germany
b Institute I for Anatomy, University of Cologne, Joseph-Stelzmann-Str. 9, 50924 Cologne, Germany
c Department of Molecular and Cellular Medicine, German Sports University, Cologne, Germany

*Corresponding author. Tel.: +49 221 478 6043; fax: +49 221 478 5906.

E-mail address: uwe.fischer{at}uk-koeln.de (U.M. Fischer).

Nuclear factor kappa-B (NF{kappa}B), a transcription factor, plays a role in numerous pathological states such as myocardial ischemia–reperfusion (I/R), apoptosis, and ischemic preconditioning. As both myocardial ischemia and reperfusion (by reactive oxygen intermediates) can activate NF{kappa}B, we investigated the impact of the antioxidant N-acetylcysteine (NAC) on NF{kappa}B-regulation in patients subjected to cardioplegic arrest (CA) on cardiopulmonary bypass (CPB). Seventeen coronary artery surgery patients (66±9[S.D.] years) subjected to cardiopulmonary bypass (CPB) and cardioplegic arrest were randomized in a double-blind fashion to receive either NAC (100 mg/kg into CPB prime followed by infusion at 20 mg/kg/h; n=9) or placebo (n=8). Transmural LV biopsies were collected prior to CPB (baseline) and at CPB-end and immuno-cytochemically stained against active NF{kappa}B and phosphorylated I{kappa}B{alpha} (activates NF{kappa}B). At the end of CPB both NF{kappa}B and I{kappa}B{alpha} were unchanged in endothelial cells of controls compared to baseline (45.6±7.6 vs. 49.9±7.1 and 36.8±6.1 vs. 47.5±8.6 counts per viewfield (cpv), P>0.05, respectively). In NAC, NF{kappa}B and I{kappa}B{alpha} in endothelial cells were significantly decreased at CPB-end (19.8±1.7 vs. 39.1±4.1 cpv, P<0.001, and 22.1±1.9 vs. 38.3±4.4 cpv, P=0.006). In cardiomyocytes, however, there were no changes observed in either group. Antioxidative treatment with NAC decreases NF{kappa}B-activity follwing I/R in endothelial cells. We conclude that NF{kappa}B-activity post I/R is mediated by free radicals rather than ischemia alone.

Key Words: Nuclear factor kappa-B; Oxidative stress; Ischemia–reperfusion; Cardiopulmonary bypass; Cardioplegic arrest; Antioxidants

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