Hemoglobin leaked from red blood cells after a brain hemorrhage in infants born too early likely contributes to the development of long-term complications often developing in the children, such as cerebral palsy.
The findings of the study, “High Presence of Extracellular Hemoglobin in the Periventricular White Matter Following Preterm Intraventricular Hemorrhage,” published in the journal Frontiers in Psychology, offer a wider understanding of the mechanisms leading to brain damage in preterm infants who experience brain bleeding.
About 15 to 20 percent of infants born too early suffer from bleeding into the fluid-filled cavities of the brain, called ventricles. This cerebral intraventricular hemorrhage causes dilation of the ventricles followed by neurological problems in about 50 percent of the infants. In addition to cerebral palsy, intellectual disabilities are also common in these cases.
Although the accumulation of blood in the ventricles is known to increase the pressure inside the brain and can lead to changes in brain anatomy, little is known about the molecular processes that contribute to brain damage.
Earlier studies have shown that red blood cells burst after a brain hemorrhage, releasing hemoglobin. Free hemoglobin easily releases its heme group, which on its own is a very reactive molecule that causes oxidative damage to fats, proteins, and DNA in cells, making it a suitable candidate for mediating tissue damage.
Researchers at Lund University in Sweden used an animal model of the condition, which they analyzed 72 hours after the bleeding. The team stained brain tissue using molecular dyes to explore how hemoglobin had spread in the brain. Using electron microscopy — a method allowing very high magnification and resolution — researchers could confirm that the hemoglobin was not inside red blood cells.
Along with the hemoglobin staining, researchers also looked for oxidative activity linked to hemoglobin. The team found that free hemoglobin and oxidative activity had spread in the brain tissue surrounding the ventricles, particularly in areas with high brain plasticity, supporting the idea that oxidative damage of tissue contributes to the development of neurological damage in infants.
The team concluded in their report that their “findings support that extracellular hemoglobin may contribute to the pathophysiological processes that cause irreversible damage to the immature brain following IVH [intraventricular hemorrhage].”
The authors believe that in the long-term, these insights might lead to efforts to develop medications that one day may prevent brain damage in these children.