title: Pharmacological neuroprotection after perinatal asphyxia.
abstract: Recent progress has provided us with several promising neuroprotective compounds to reduce perinatal hypoxic-ischemic (HI) brain injury. In the early post HI phase, therapies can be concentrated on ion channel blockage (Xenon), anti-oxidation (allopurinol, 2-iminobiotin, and indomethacin), anti-inflammation (erythropoietin [EPO], melatonin), and anti-apoptosis (nuclear factor kappa B [NF-&#x03BA;B]and c-jun N-terminal kinase [JNK] inhibitors); in the later phase, therapies should be targeted to promote neuronal regeneration by stimulation of neurotrophic properties of the neonatal brain (EPO, growth factors, stem cells transplantation). Combination of pharmacological interventions with moderate hypothermia, which is the only established therapy for post HI brain injury, is probably the next step to fight HI brain damage in the clinical setting. Further studies should be concentrated on more rational pharmacological strategies by determining the optimal time and dose to inhibit the various potentially destructive molecular pathways and/or to enhance endogenous repair meanwhile avoiding the adverse effects.
authors.affiliation: Department of Neonatology, University Medical Center, Utrecht, The Netherlands.
authors.forename: Xiyong
authors.initials: X
authors.lastname: Fan
authors.forename: Frank
authors.initials: F
authors.lastname: van Bel
mesh_terms: D001238:Asphyxia Neonatorum / Q000188:drug therapy* / Q000503:physiopathology; D003131:Combined Modality Therapy; D019610:Cytoprotection / Q000187:drug effects*; D006801:Humans; D007231:Infant, Newborn; D015931:Intensive Care, Neonatal / Q000379:methods / Q000639:trends; D009359:Neonatology / Q000379:methods / Q000639:trends*; D018696:Neuroprotective Agents / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use*
chemical_list: D018696:Neuroprotective Agents