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Eur J Cardiothorac Surg 1999;16:32-37
© 1999 Elsevier Science NL
a Yorkshire Heart Centre, Leeds General Infirmary, Leeds, UK
b Walsgrave Hospital and the University of Warwick, Coventry, UK
Corresponding author. Morriston Hospital NHS Trust, Morriston, Swansea SA6 6NZ UK. Tel.: +44-1792-704126; fax: +44-1792-704141
Objectives: Neurological damage following cardiopulmonary bypass (CPB) is difficult to objectively evaluate in infants. In adults, serum elevations of astroglial S100B correlate with proven brain injury independent of operative temperature. The deleterious effects of inflammatory cytokines, generated during CPB, on the brain have not been studied in infants using S100B as a marker for cerebral injury. Methods: Twelve neonates, weighing 3.3±0.2 kg (total circulatory arrest group (TCA)) and 12 infants weighing 7.0±1.0 kg (cardiopulmonary bypass group (CPB)) underwent corrective cardiac surgery for various pathologies. Serial blood samples on induction, at the end of CPB, 30 min, 2 h and 24 h after the administration of protamine, were taken. The resultant plasma was frozen to -80°C and stored for batch analysis. Cytokines were measured using ELISAs and S100B using a luminometric assay. Results: The TCA group were younger and experienced a longer perfusion time than the CPB group (137±8 vs. 113±7, P=0.04). The mean TCA time was 23±4 min. The TCA group had significantly higher levels of IL-6 (P=0.001), IL-8 (P=0.005)and S100B (P=0.002) at 24 h. C5b-9 levels were significantly lower in the TCA group: end of CPB (P=0.001), 30 min (P<0.001), 2 h (P=0.002). There was a weak, but significant correlation between IL-6 levels at the end of CPB and S100B levels 2 h later (r=0.55, P=0.03). Long extubation times were associated with high 24-h S100B levels (r=0.52, P=0.01). Conclusions: (1) The TCA group have prolonged rises of IL-6, IL-8 and S100B. (2) The TCA group generates significantly lower complement. (3) Astroglial injury, seen after surgery, may, in part, be cytokine mediated.
Key Words: Cerebral injury • S100B • Cytokines • Inflammation
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