OBJECTIVE: The incidence of bilirubin encephalopathy in extremely ill neonates with low serum bilirubin is stimulating interest in factors that can modify the blood-brain barrier permeability and allow the passage of bilirubin-albumin macrocomplexes, which may be produced by hypercapnia. MATERIALS AND METHODS: Without modifying the normal bilirubin-albumin affinity, we increased cerebral flow by two levels of hypercapnia (PCO2 67.1 and 101.9 mmHg), acquired by inhalation of CO2 enriched air (5 and 15%) and a decrease in pH (7.00 and 6.93). RESULTS: We demonstrate an increment in cerebral bilirubin deposition (control 2.43 +/- 0.54 mg/g versus 3.29 +/- 0.43 and 3.28 +/- 1.07, F = 4.80, p < 0.05) and I125 albumin (control 26.1 +/- 95.8 micrograms/g versus 364.4 +/- 156.1 and 430.8 +/- 122.4, F03.34, p < 0.05).
OBJECTIVE: The incidence of bilirubinencephalopathy in extremely ill neonates with low serum bilirubin is stimulating interest in factors that can modify the blood-brain barrier permeability and allow the passage of bilirubin-albumin macrocomplexes, which may be produced by hypercapnia. MATERIALS AND METHODS: Without modifying the normal bilirubin-albumin affinity, we increased cerebral flow by two levels of hypercapnia (PCO2 67.1 and 101.9 mmHg), acquired by inhalation of CO2 enriched air (5 and 15%) and a decrease in pH (7.00 and 6.93). RESULTS: We demonstrate an increment in cerebral bilirubin deposition (control 2.43 +/- 0.54 mg/g versus 3.29 +/- 0.43 and 3.28 +/- 1.07, F = 4.80, p < 0.05) and I125 albumin (control 26.1 +/- 95.8 micrograms/g versus 364.4 +/- 156.1 and 430.8 +/- 122.4, F03.34, p < 0.05).