Neuroprotective effect of selective antegrade cerebral perfusion during prolonged deep hypothermic circulatory arrest: Cerebral metabolism evidence in a pig model.

OBJECTIVE

The aim of this study was to elucidate the mechanism of cerebral injury and to evaluate selective antegrade cerebral perfusion (SACP) as a superior neuroprotective strategy for prolonged deep hypothermic circulatory arrest (DHCA).

METHODS

Twelve pigs (6-8-week old) were randomly assigned to DHCA alone (n=6) and DHCA with SACP (n=6) at 18°C for 80 min groups. Serum S100 was determined using an immunoassay analyzer. The concentrations of cerebral dialysate glucose, lactate, pyruvate, glycerol, and glutamate were measured using a microdialysis analyzer.

RESULTS

Compared with a peak at T4 (after 60 min of rewarming) in the DHCA group, the serum S100 in the SACP group was significantly lower throughout the study. The DHCA group was susceptible to significant increases in the levels of lactate, glycerol, and glutamate and the ratio of lactate/pyruvate as well as decreases in the level of glucose. These microdialysis variables showed only minor changes in the SACP group. There was a positive correlation between cerebral lactate and intracranial pressure during reperfusion in the DHCA group. However, the apoptosis index and C-FOS protein levels were lower in the SACP group.

CONCLUSION

Metabolic dysfunction is involved in the mechanism of cerebral injury. SACP is a superior neuroprotective strategy for both mild and prolonged DHCA.