رسالة جامعية

Neurovascular and mitochondrial dysfunctions in a neonatal rat stroke model ; Dysfonctions neurovasculaires et mitochondriales dans un modèle néonatal d'ischémie cérébrale focale

التفاصيل البيبلوغرافية
العنوان: Neurovascular and mitochondrial dysfunctions in a neonatal rat stroke model ; Dysfonctions neurovasculaires et mitochondriales dans un modèle néonatal d'ischémie cérébrale focale
المؤلفون: Leger, Pierre-Louis
المساهمون: Physiopathologie, conséquences fonctionnelles et neuroprotection des atteintes du cerveau en développement, Université Paris Diderot - Paris 7 (UPD7)-IFR2-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris VI, Christiane Charriaut-Marlangue
المصدر: https://theses.hal.science/tel-00833157Test ; Neurosciences [q-bio.NC]. Université Pierre et Marie Curie - Paris VI, 2012. Français. ⟨NNT : 2012PAO66561⟩.
بيانات النشر: HAL CCSD
سنة النشر: 2012
مصطلحات موضوعية: Neonatal focal cerebral ischemia, reperfusion injury, mitochondrial mPTP pore, ischemic postconditioning, mitochondrial respiration, early reperfusion, collateral circulation, cerebral microcirculation, regional reperfusion, ischémie cérébrale focale néonatale, lésions de la reperfusion, Ciclosporine A, pore mitochondrial mPTP, Postconditionnement ischémique, respiration mitochondriale, reperfusion précoce, circulation collatérale, microcirculation cérébrale, reperfusion régionale, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
الوصف: We evaluated Ciclosporine A effect on brain lesions, and afterwards we explored the mitochondrial metabolism. We have studied the ischemic postconditioning neuroprotective effects and the hemodynamic consequences of the reperfusion. We have shown the mitochondrial permeability transition pore was opened during neonatal ischemia. Ciclosporine A increased calcium reuptake into mitochondria, but also improved the mitochondrial respiration. Ciclosporine A limited the inflammatory processes during ischemia. However, CsA did not reduce the volume of brain lesions. In conclusion, we have shown that Cyclophiline D and the mPTP pore were two major elements in neonatal cerebral ischemia. We have also explored the ischemic postconditioning neuroprotective effects. We did not show a decrease in brain lesions. Nevertheless, we have demonstrated that reperfusion was different in neonatal and adult models, because of a gradual and slow reperfusion in the early reperfusion phase, instead of hyperemia. We have highlighted that the reperfusion had the same kinetic profile in both hemispheres, concerning superficial cortical perfusion and deep cerebral perfusion. We concluded that cerebral vasoconstriction was the sign of the cerebral microcirculation dysfunction. The microcirculation was altered in neonatal cerebral ischemia but differently than in adult models. The early collateral recruitment could explain these differences ; Nos travaux de recherche menés dans l'ischémie cérébrale néonatale ont évalué l'effet de la Ciclosporine A sur la réduction du volume lésionnel, mais aussi sur le fonctionnement du métabolisme mitochondrial. Nous avons également étudié l'effet du postconditionnement ischémique et les conséquences hémodynamiques de la reperfusion. Le pore de perméabilité membranaire mPTP s'ouvre au cours de l'ischémie néonatale. La CsA, inhibiteur de la Cyclophiline D freine l'ouverture du pore mPTP, améliore la capacité de recapture du calcium par la mitochondrie, la respiration mitochondriale, et limite les effets ...
نوع الوثيقة: doctoral or postdoctoral thesis
اللغة: French
العلاقة: NNT: 2012PAO66561; tel-00833157; https://theses.hal.science/tel-00833157Test; https://theses.hal.science/tel-00833157/documentTest; https://theses.hal.science/tel-00833157/file/ThA_se_LEGER_Pierre-Louis_NA_Etudiant_UPMC_2507042.pdfTest
الإتاحة: https://theses.hal.science/tel-00833157Test
https://theses.hal.science/tel-00833157/documentTest
https://theses.hal.science/tel-00833157/file/ThA_se_LEGER_Pierre-Louis_NA_Etudiant_UPMC_2507042.pdfTest
حقوق: info:eu-repo/semantics/OpenAccess
رقم الانضمام: edsbas.1BC8DFC5
قاعدة البيانات: BASE