• Media type: E-Article
  • Title: Magnesium sulfate treatment decreases the initial brain damage alterations produced after perinatal asphyxia in fetal lambs
  • Contributor: Goñi‐de‐Cerio, Felipe; Alvarez, Antonia; Lara‐Celador, Idoia; Alvarez, Francisco J.; Alonso‐Alconada, Daniel; Hilario, Enrique
  • imprint: Wiley, 2012
  • Published in: Journal of Neuroscience Research
  • Language: English
  • DOI: 10.1002/jnr.23091
  • ISSN: 0360-4012; 1097-4547
  • Keywords: Cellular and Molecular Neuroscience
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title><jats:p>The aim of this work was to analyze the effect of MgSO<jats:sub>4</jats:sub> treatment in the brain after hypoxic–ischemic (HI) injury in premature fetal lambs. Injury was induced by partial occlusion of umbilical cord for 60 min, and then the preterm lambs (80–90% of gestation) were randomly assigned to one of the following groups: control group, in which the animals were managed by conventional mechanical ventilation for 3 hr; 3 hr postpartial cord occlusion (3‐hr‐PCO) group, in which injured animals were managed by ventilation and then sacrificed 3 hr after HI; and MgSO<jats:sub>4</jats:sub> group, in which animals received 400 mg/kg MgSO<jats:sub>4</jats:sub> for 20 min soon after HI was induced and were managed by ventilation for 3 hr. Brains were analyzed for apoptosis by TUNEL assay. Cell viability and intracellular state studies were assessed by flow cytometry. The delayed death index was significantly increased in the 3‐hr‐PCO group in comparison with control. Administration of MgSO<jats:sub>4</jats:sub> elicited a delay in cell death that was similar to that in the control group. The 3‐hr‐PCO group showed a significantly higher concentration of reactive oxygen species, mitochondrial damage, and intracellular calcium in comparison with control and MgSO<jats:sub>4</jats:sub>‐ treated groups. Our results suggest that MgSO<jats:sub>4</jats:sub> treatment might have potential therapeutic benefits after the HI event. © 2012 Wiley Periodicals, Inc.</jats:p>