ABSTRACT
The aim of this study was to evaluate the relationship between the kinetic patterns of the protein S-100beta, an astroglial cell marker, and its immunohistochemical expression in the brain in rabbits that underwent cardiopulmonary bypass with deep hypothermic circulatory arrest. Fourteen New Zealand rabbits (weight, 3.1+/-0.25 kg) were anaesthetised, intubated and mechanically ventilated. Four animals were not connected to the cardiopulmonary bypass and served as controls. Ten animals were perfused according to a uniform protocol. After systemic cooling, deep hypothermic circulatory arrest was induced for 60 minutes. After reperfusion and rewarming, the animals were weaned from bypass and sacrificed. In the brain, astrocyte reactivity for S-100beta was evaluated immunocytochemically (DPC Immustain) and the serum concentrations of S-100beta were analysed using a commercially available immunoluminometric kit (Byk-Sangtec, Dietzenbach, Germany). In all experimental animals a significant increase of the serum concentration of the protein S-100beta was found immediately after reperfusion and the termination of cardiopulmonary bypass. In comparison with the control animals, increased staining of S-100beta was found in the astroglial cells and swollen astrocytic end-feet in the perivascular regions. There were fewer signs of neuronal cell injury of neurones in the hippocampus structure. In conclusion, astrocytic activation and S-100beta overexpression seems to precede the neurodegeneration following deep hypothermic circulatory arrest. The marked perivascular cell swelling may support the assumption of reperfusion injury of the astroglial cell complex that forms the blood-brain barrier, which may be indicative of the source of the released S-100beta into the blood stream.
