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307 Effects of the Ischemic Postconditioning in A Neonatal Stroke Model
  1. PL Leger1,2,
  2. P Bonnin3,
  3. S Renolleau1,2,
  4. O Baud1,4,
  5. C CharriautMarlangue1
  1. 1Neurosciences Research Unit, INSERM U676- Paris Diderot University- Paris VII
  2. 2Pediatric Intensive Care Unit, Armand Trousseau Hospital - APHP- UPMC University- Paris VI
  3. 3Cardiovascular and Physiology Research Unit, INSERM U965- Lariboisiere Hospital- Paris Diderot University- Paris VII
  4. 4Neonatal Intensive Care Unit, Robert Debré Hospital - APHP, Paris, France


The lack of efficient neuroprotective strategies for neonatal stroke could be ascribed to pathogenic ischemic processes differentiating adults and neonates. In the present study, we tested the hypothesis that ischemic postconditioning applied immediately after ischemia provides neuroprotection in a neonatal stroke model. Neonatal ischemia was generated by permanent occlusion of the left distal middle cerebral artery combined with 50 min of occlusion of both common carotid arteries (CCA) in P7 rats. Postconditioning was performed by repetitive brief release and occlusion (30 s, 1 or 5 min) of CCA after 50 min of CCA occlusion. Alternative reperfusion was generated by controlled release of the bilateral CCA occlusion. Blood-flow velocities in the left internal carotid artery were measured using ultrasound imaging with sequential Doppler recordings. Cortical perfusion was measured using laser Doppler. Local cerebral blood-flow was measured by iodo[14C]antipyrine autoradiography. None of the procedures of serial mechanical interruptions of blood flow applied at reperfusion induced a reduction of infarct volume after 72 hours. In contrast to adult ischemia, a gradual perfusion was found during early re-flow both in the left internal carotid artery and in the cortical penumbra. No hyperemia was detected on autoradiograms. In addition, vasodilation to hypercapnia remained unchanged. Absence of acute hyperemia during early CCA re-flows and absence of increased cerebrovascular reactivity could at least in part explain the inefficiency of ischemic postconditioning in the developing brain.

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