Does antegrade cerebral perfusion protect the brain during deep hypothermic circulatory arrest?

This study compares cerebral protection using no cerebroplegia and using antegrade cerebroplegia with variable flow rates during deep hypothermic circulatory arrest (DHCA).

Twenty healthy neonatal piglets (2.5-3.8 kg) underwent 60 minutes of DHCA. No cerebroplegia was used in group 1 (n = 5). Cold (16 degrees C) antegrade cerebral perfusate was administered through the innominate artery at 10 mL/kg per minute in group 2 (n = 5), at 25 mL/kg per minute in group 3 (n = 5), and at 50 mL/kg per minute in group 4 (n = 5). Venous samples for lactate, pyruvate, S-100B protein, and creatine kinase BB (CKBB) were drawn from the jugular vein before and after discontinuation of cardiopulmonary bypass--lactate at 5 minutes postbypass, pyruvate at 5 minutes postbypass, S-100B protein at 30 minutes postbypass, and CKBB at 6 hours postbypass. Piglets were killed 6 hours postbypass and their brains were harvested for histological/immunologic studies. Extent of damage was assessed using a semiquantitative score of 0 to 4 based on a validated method.

Evidence for significant apoptosis and necrosis was apparent in all groups. The mean H&E score was 2.2 for group 1, 2.3 for group 2, 2.5 for group 3, and 2.3 for group 4. The mean terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling score was 1.0 for group 1, 1.2 for group 2, 1.7 for group 3, and 0.8 for group 4. Pathological changes were not greater in the piglets that did not have antegrade cerebral perfusion. Serum lactate, pyruvate, S-100B protein, and CKBB did not distinguish between perfusion strategies.

In neonates, unmodified antegrade cerebral perfusion at flow rates of 10, 25, and 50 mL/kg per minute during DHCA does not provide additional protection of the brain as determined by histology, immunology, serum lactate, pyruvate, S-100B protein, and CKBB.