- Meeting abstract
- Open Access
Free radicals induced lipid peroxidation following reperfusion in infants cardiac surgery: relationship to the release of the brain marker protein S-100 into the serum
© Current Science Ltd 1999
- Published: 2 March 1999
- Membrane Injury
- Maximal Serum Concentration
- Potential Therapeutic Application
- Increase Cell Membrane
- Acid Adduct
Measurement of malondialdehyde (MDA) in the serum, as a marker of free radical induced lipid peroxidation may provide possible information on radicals accentuated structural membrane injury. The detection of protein S-100 in serum, which is exclusively specific for cytoplasma of astroglial and Schwann cells in association with extracorporeal perfusion, may quite possibly indicate either an increased cell membrane permeability or cell injury. The aim of this study therefore was to evaluate the serum kinetics of protein S-100 in relationship to possible free radicals mediated cerebral membrane injury in infants undergoing cardiac surgery by means of cardiopulmonary bypass (CPB).
56 patients (neonate n = 7, infants n = 16, children n = 23) were enrolled in this study. Cardiac surgery was performed using full-flow CPB (120-150 ml/kg/min), minimal rectal temperature (26 ± 7.5°C), and minimal hemoglobin concentration (7.4 ± 1.1 mg/dl). Total circulatory arrest was not used. Blood samples were collected from the same venous line at the following intervals: before CPB, 10 min. after CPB start, 10 min after aortic cross clamping, during CPB, 5min following declamping of the aorta. The blood samples were treated separately immediately after collection. The S-100 protein serum concentrations were analyzed using a commercially available LIA kit (Sangtec® Medical AB, Bromma, Sweden). MDA was measured (MDA-thiobarbituric acid adduct) using HPLC.
In comparison to the pre-bypass values, a significant increase in the concentration of protein S-100 was found immediately after the start of CPB (P = 0.01). There was a continuous elevation of the concentration of protein S-100 in the following phases of CPB. However, the main release of protein S-100 was found in the reperfusion phase after the declamping of the aorta and the end of CPB (P = 0.0001). In comparison to the pre-bypass values the serum concentrations of malondialdehyde were decreased 5 minutes after cross clamping of the aorta (P = 0.001). Parallel to the increase of protein S-100 concomitant elevation of serum MD were also found following the declamping of the aorta and after the end of CPB (P = 0.0003).
The maximal serum concentrations of protein S-100 correlated significantly to bypass time (r = 0.7, P = 0.0007), cross-clamping time (r = 0.57, P = 0.001) and minimal rectal temperature during CPB (-0.57, P = 0.001). The maximal MDA values correlated significantly to cross-clamping time (r = 0.46, P = 0.004) and minimal rectal temperature (r = 0.40, P = 0.007).
The concomitant elevation of the concentration of MDA and the astroglial cell marker S-100 could support the view of the role of free-radicals mediated transient ischemia reperfusion membrane injury in the cerebral endothelial microvascular. These observations may have potential therapeutic applications to preserve and protect cellular and tissue function in clinical conditions