Brain apoptosis and carotid artery reactivity in fetal asphyctic preconditioning

Eveline Strackx, Bea Zoer, Daniel Van den Hove, Hellen Steinbusch, Harry Steinbusch, Carlos Blanco, Johan S H Vles, Eduardo Villamor, Antonio Wenceslao Danilo Gavilanes

Research output: Contribution to journalArticleAcademicpeer-review


We aimed to develop a model of fetal hypoxia-ischemia (HI) preconditioning that reflects the pathophysiological conditions of perinatal asphyxia more closely than the existing neonatal stroke models. Fetal asphyxia (FA) was induced by clamping the uterine vasculature on embryonic day E17. At birth (P0), severe perinatal asphyxia (SPA) was induced during cesarean section. At P4, carotid arteries were studied in a wire myograph and at P8 brains were analyzed for apoptotic cell death in the prefrontal cortex and striatum. The contraction induced by K+ was significantly reduced in the carotid arteries from the SPA group and endothelium-dependent relaxation (mediated by acetylcholine) was augmented in the FA group. These changes in vascular responsiveness were not present in the animals exposed to both insults (FA + SPA). Additionally, FA+SPA animals showed lower numbers of apoptotic cells compared to SPA animals in both the prefrontal cortex and striatum. Exposure to a global fetal asphyctic insult seems to protect against the vascular alterations and the increase of apoptosis in striatum and prefrontal cortex induced by severe asphyxia at birth.

Original languageEnglish
Pages (from-to)781-90
Number of pages10
JournalFrontiers in bioscience - scholar edition
Issue number2
Publication statusPublished - 1 Jan 2010


  • 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
  • Analysis of Variance
  • Animals
  • Apoptosis
  • Brain
  • Carotid Arteries
  • Disease Models, Animal
  • Fetal Hypoxia
  • Hypoxia-Ischemia, Brain
  • In Situ Nick-End Labeling
  • Ischemic Preconditioning
  • Rats
  • Rats, Sprague-Dawley
  • Vasoconstriction
  • Journal Article

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