Free hemoglobin impairs cardiac function in neonatal rabbit hearts

Hemolysis caused by cardiopulmonary bypass causes renal dysfunction and other organ failure presumably by superoxide production catalyzed by iron derived from free hemoglobin (f-Hb). It might also impair cardiac function by the same mechanism, especially in the ischemia-reperfusion period and in neonates where serum antioxidant activity is lower than adults.

We evaluated effects of f-Hb on cardiac function with or without ischemia and reperfusion using a newborn (7 days old) rabbit crystalloid-perfused Langendorff model. After baseline measurements, the hearts were divided into the following four groups (8 hearts per group): (1) those perfused with regular Krebs-Henseleit bicarbonate buffer, (2) those perfused 30 minutes with KH buffer containing 1 mg/mL of f-Hb obtained from osmotic hemolysis, (3) those subjected to 180 minutes of cold global ischemia with infusion of crystalloid cardioplegia and reperfused with Krebs-Henseleit buffer, and (4) those subjected to the same ischemia and reperfused with Krebs-Henseleit buffer containing 1 mg/mL of f-Hb. The left ventricular function (using conductance catheter and isovolumic balloon) and coronary flow were measured.

Free hemoglobin significantly impaired not only left ventricular function but also coronary flow even without ischemia (p < 0.05). When ischemia and reperfusion were involved, the group reperfused with f-Hb showed the worst left ventricular function and coronary flow among the groups.

This study shows that f-Hb directly impaired cardiac function and coronary flow in neonatal hearts especially in ischemia and reperfusion.