Hemoglobin induces inflammation after preterm intraventricular hemorrhage by methemoglobin formation.

ABSTRACT:

Background

Cerebral intraventricular hemorrhage (IVH) is a major cause of severe neurodevelopmental impairment in preterm infants. To date, no therapy is available that prevents infants from developing serious neurological disability following IVH. Thus, to develop treatment strategies for IVH, it is essential to characterize the initial sequence of molecular events that leads to brain damage. In this study, we investigated extracellular hemoglobin (Hb) as a causal initiator of inflammation in preterm IVH.

Methods

Using a preterm rabbit pup model, we investigated the molecular mechanisms and events following IVH. We also characterized the concentrations of cell-free Hb metabolites and pro-inflammatory mediators in the cerebrospinal fluid (CSF) of preterm human infants and ra

SUBMITTER: Gram M 

PROVIDER: S-EPMC3750409 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature