Post hypoxic-ischemic (HI) reperfusion induces liberation of non-protein-bound iron from its binding proteins (NPBI), leading to formation of hydroxyl radicals and has been associated with post-HI injury of the brain. Reperfusion injury has been characterized by post-asphyxial cerebral hypoperfusion, a decreased cerebral O2 consumption (CMRO2) and electrocortical brain activity (ECBA).

Aim: We investigated the effect of the iron-chelator DFO on brain perfusion/CMRO2/ECBA.

Study design: We induced severe HI in 14 newborn lambs and measured changes (%) from pre-HI values, at 15, 60, 120 and 180 min after HI of carotid artery flow (Qcar [mL/min]), CMRO2 and ECBA [μV]. Immediately after the completion of HI insult, 7 lambs received a placebo(CONT), and 7 received DFO (2.5 mg/kg).

Results: Qcar-CONT was significantly decreased at 60 °, 120°, 180 ° min post-HI vs Qcar-DFO and at 120 °, 180 ° min post-HI vs pre-HI values. CMRO2-CONT decreased significantly vs pre-HI values at 60 °, 120 ° and vs DFO at 180 ° min post-HI. ECBA-CONT decreased significantly up to 40% vs pre-HI values, without recovery. ECBA-DFO remained stable during the study period.

Conclusions: Preservation of post-HI Qcar, CMRO2, and ECBA in DFO treated lambs suggests that chelation of NPBI, immediately after HI, reduces post-asphyxial cerebral reperfusion injury.