Delayed Hypoxic Postconditioning Protects Against Cerebral Ischemia in the Mouse

• DOI: 10.1161/strokeaha.109.557314
• Publication Date: 2009-07-24T02:06:05Z
• Authors: Claire Leconte; Emmanuelle Tixier; Thomas Freret; Jérôme Toutain; Romaric Saulnier; Michel Boulouard; Simon Roussel; Pascale Schumann-...; Myriam Bernaudin
• Keywords: Adrenomedullin; Hypoxia; Stroke

Background and Purpose— Inspired from preconditioning studies, ischemic postconditioning, consisting of the application intermittent interruptions blood flow shortly after reperfusion, has been described in cardiac ischemia recently stroke. It is well known that tolerance can be achieved brain not only by preconditioning, but also hypoxic preconditioning. However, existence postconditioning never reported cerebral ischemia. Methods— Adult mice subjected to transient middle artery occlusion underwent chronic hypoxia starting either 1 or 5 days damage was assessed T2-weighted MRI at 43 days. In addition, we investigated potential neuroprotective effect applied oxygen glucose deprivation primary neuronal cultures. Results— The present study shows for first time a late (5 days) reduced delayed thalamic atrophy. Furthermore, performed 14 hours induced neuroprotection We found hypoxia-inducible factor-1α expression as those its target genes erythropoietin adrenomedullin increased postconditioning. Further studies with pharmacological inhibitors recombinant proteins revealed these molecules participate this postconditioning-induced neuroprotection. Conclusions— Altogether, demonstrates vitro highlight genes, adrenomedullin, effectors