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DOI: 10.1177/1933719107305864 Neuroprotective Effect of Long-term MgSO4 Administration After Cerebral Hypoxia-Ischemia in Newborn Rats Is Related to the Severity of Brain DamageDepartment of Physiology and Pharmacology Faculty of Medicine, Aristotle University of Thessaloniki Thessaloniki, Greece, spandou{at}med.auth.gr
Department of Neonatology Facuty of Medicine, Aristotle University of Thessaloniki Thessaloniki Greece
Department of Physiology and Pharmacology Faculty of Medicine, Aristotle University of Thessaloniki Thessaloniki, Greece
Department of Pediatrics Faculty of Medcine, Aristotle University of Thessloniki, Thessloniki, Greece
Department of Physiology and Pharmacology Faculty of Medicine, Aristotle University of Thessaloniki Thessaloniki, Greece
Department of Physiology and Pharmacology Faculty of Medicine, Aristotle University of Thessaloniki Thessaloniki, Greece
Department of Pathology Faculty of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece
Department of Physiology and Pharmacology Faculty of Medicine, Aristotle University of Thessaloniki Thessaloniki, Greece Previous studies have shown contradictory results regarding magnesium-mediated neuroprotection in animal models of perinatal asphyxia. The aim of this study is to investigate the e fects of MgSO4 postasphyxial treatment on hypoxia-ischemia (HI)—induced brain injury in neonatal rats and the possibility that this e fect is related to the severity of brain damage. Seven-day-old rats underwent unilateral carotid artery ligation followed by 1 or 2 hours of hypoxia (8% O2) and MgSO4 administration. Adenosine triphosphate/phosphocreatine and glutamate/glutamine measurements and neuropathological evaluation of the hippocampus were used to assess the e fects of HI and MgSO4. HI caused time-dependent changes in energy stores, amino acid concentrations, and brain damage. Administration of MgSO4 after 1 hour but not after 2 hours of hypoxia resulted in significant prevention of HI-induced brain injury. MgSO4 administration results in a significant protection against moderate HI-induced brain damage, whereas it fails to offer a similar effect against severe brain damage.
Key Words: Magnesium sulfate hypoxia-ischemia newborn rat hippocampus.
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