Nitric oxide production affects cerebral perfusion and metabolism after deep hypothermic circulatory arrest

Background Use of deep hypothermic circulatory arrest (DHCA) in infant cardiac surgery is associated with reduced cerebral perfusion and metabolism during the recovery period. We investigated the impairment of nitric oxide production as a possible cause. Methods A group of 1-week-old piglets underwent normothermic cardiopulmonary bypass (group A); three other groups (B, C, and D; n = 6 per group) underwent 60 minutes of DHCA at 18°C and 60 minutes of rewarming. The animals were then treated as follows: Groups A and B received l-ω-nitro-arginine-methyl-ester (l-NAME, 50 mg · kg−1); group C, saline solution; and group D, l-arginine (600 mg · kg−1). Results In group A, global cerebral blood flow decreased to 37.3% ± 4.2% of baseline after l-NAME administration (p < 0.005). In group B, global cerebral blood flow decreased to 44.6% ± 4.4% of baseline after DHCA and 28.9% ± 3.4% after l-NAME administration (p < 0.001). Following l-arginine treatment after DHCA (group D), global cerebral blood flow increased from 43.8% ± 3.0% of baseline to 61.6% ± 9.1% (p < 0.05); cerebral oxygen metabolism increased from 1.93 ± 0.16 mL · min−1 · 100 g−1 after DHCA to 2.42 ± 0.25 mL · min−1 · 100 g−1 (p < 0.05). Conclusions Tonal production of nitric oxide is impaired in the brain after DHCA and is partly responsible for the circulatory and metabolic changes observed. Stimulation of nitric oxide production (l-arginine) significantly improved recovery of cerebral blood flow and cerebral oxygen metabolism after DHCA.