Revista argentina de cardiología
versión On-line ISSN 1850-3748
MILEI, José et al. Formation of Reactive Oxygen Species during Post Ischemic Reperfusion. Ultrastructural Damage. Rev. argent. cardiol. [online]. 2006, vol.74, n.1, pp. 12-18. ISSN 1850-3748.
Background Formation of reactive oxygen species during post ischemic reperfusion in experimental models induces "oxidative stress", which may exert deleterious effects on myocardium. Since during cardioplegic arrest patients undergo ischemia/ reperfusion, it has been proposed that oxidative stress might occur during cardiac surgery. However, this phenomenon has not been yet fully characterized. Study Aim To correlate glutathione release (the initial step of oxidative stress) with markers of progression of oxidant injury, such as peroxidation of membrane lipids and development of ultrastructural alterations. Methods and Results We systematically investigated changes in several markers of oxidative stress and tissue injury occurring during post ischemic reperfusion in 24 patients undergoing coronary artery bypass. Trans-cardiac blood sampling and tissue biopsies were taken at baseline and after reperfusion following an average 40.9±11.9 min cardioplegic arrest. Glutathione release was negligible at baseline (0.02±0.04 µmol/ L), but markedly increased 15 min after reperfusion (1.10±0.40 µmol/L; p< 0.05); concurrently, tissue concentration of the antioxidant ubiquinol decreased from 144.5±52.0 to 97.6±82.0 nmol/g (p< 0.05). Even though these changes document exposure of the heart to oxidants, this was not accompanied by biochemical alterations indicative of cell injury, since neither coronary sinus blood nor cardiac biopsies showed increased lipid peroxidation. Furthermore, electron microscopy showed no major ultrastructural alterations. Conclusions Although an excess of oxidant production occurs in patients undergoing cardiac surgery, in our settings, cardiac oxidative stress did not progress to membrane damage and irreversible injury.
Palabras llave : Cardiac surgery; Oxidative stress; Reperfusion injury; Coronary artery bypass; Myocardial protection.