Post hypoxic-ischemic (HI) reperfusion induces excess production of non protein bound iron (NPBI), leading to formation of the highly reactive hydroxyl radical. We investigated if the iron-chelator DFO could reduce reperfusion injury and improve left ventricular (LV) function. We produced severe HI in 13 newborn lambs and measured changes from pre-HI values, at 15, 60 and 120 min after HI of the following parameters: mean arterial blood pressure (MABP), stroke work (SW) and cardiac output (CO). LV contractility and CO were assessed by measuring LV pressure (tip-manometer) and volume(conductance catheter), using inferior caval vein occlusion to obtain slope(Ees) and intercept of the end systolic PV relationship (V10). NPBI, reduced and oxidized vitamine C ratio (VCred/ox) and lipid peroxidation (MDA) were determined from sinus coronarius blood. 7 Lambs received DFO (10 mg/kg i.v.) immediately after HI, control lambs (CONT) received a placebo.

Results: MABP was stable, CO and SW decreased only in CONT. Ees and V10 decreased post HI, but did not differ between groups. NPBI and MDA were higher at 15 min post HI (p<0.05), VCred/ox was lower in CONT at 15 min post-HI (p<0.05). Figure

figure 1

Figure 1

Conclusions: Less oxidative stress and the preservation of CO and SW in DFO suggests a positive effect of iron-chelation in the postasphyxial lamb heart.