Non-protein-bound iron (NPBI) can convert hydrogen peroxide into highly reactive hydroxyl radicals and has been associated with post hypoxic-ischemic(HI) reperfusion injury of the brain. This type of injury is characterized by post-HI cerebral hypoperfusion, and decreased cerebral O2-consumption(CMRo2) and electrocortical brain activity (ECBA). We investigated if the iron chelator DFO could reduce reperfusion injury. Severe HI was induced in 12 newborn lambs and changes from pre-HI values were measured for brain blood flow (carotid flow [mL/min]; Qcar), CMRo2 and ECBA [uV] at 15, 60, 120 and 180 min after HI. Immediately after completion of HI 6 lambs received a placebo (CONT) and 6 DFO (10 mg/kg/iv). Results: CONT showed a significant decrease in Qcar (120, 180 min), CMRo2 (60,180 min) and ECBA (15-180 min) up to 60% of pre-HI levels without recovery to pre-HI-levels. In contrast, the DFO-lambs had a preservation of post-HI Qcar, CMRo2 and ECBA with significantly higher values as compared to CONT lambs (see figure). Conclusions: Preservation of post-HI cerebral perfusion, CMRo2 and ECBA in DFO-lambs suggests that chelation of NPBI with DFO, immediately after HI, prevents post-asphyxial cerebral reperfusion injury.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Shadid, M., Dorrepaal, C., Steendijk, P. et al. DEFEROXAMINE (DFO) REDUCES CEREBRAL REPERFUSION INJURY AFTER BIRTH ASPHYXIA.• 2267. Pediatr Res 39 (Suppl 4), 381 (1996). https://doi.org/10.1203/00006450-199604001-02292
Issue Date:
DOI: https://doi.org/10.1203/00006450-199604001-02292