Free hemoglobin impairs cardiac function in neonatal rabbit hearts.

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