المؤلفون: Stéphane, Gennai, Christophe, Pison, Raphaël, Briot

المصدر: Presse medicale (Paris, France : 1983). 43(9)

مصطلحات موضوعية: Carbon Monoxide, NADPH Oxidases, Apoptosis, Pulmonary Surfactants, Organ Preservation, Nitric Oxide, Mitochondrial Membrane Transport Proteins, Respiration, Artificial, Severity of Illness Index, Bronchodilator Agents, Oxygen, Pulmonary Alveoli, Oxidative Stress, Adenosine Triphosphate, Reperfusion Injury, Reperfusion, Cytokines, Humans, Calcium, Sodium-Potassium-Exchanging ATPase, Ischemic Postconditioning, Ischemic Preconditioning, Reactive Oxygen Species, Lung Transplantation

الوصف: Lung ischemia-reperfusion is characterized by diffuse alveolar damage arising from the first hours after transplantation. The first etiology of the primary graft dysfunction in lung is ischemia-reperfusion. It is burdened by an important morbi-mortality. Lung ischemia-reperfusion increases the oxidative stress, inactivates the sodium pump, increases the intracellular calcium, leads to cellular death and the liberation of pro-inflammatory mediators. Researches relative to the reduction of the lung ischemia-reperfusion injuries are numerous but few of them found a place in common clinical practice, because of an insufficient level of proofs. Ex vivolung evaluation is a suitable technique in order to evaluate therapeutics supposed to limit lung ischemia-reperfusion injuries.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=pmid________::ee61b15f29a34d8b0cd55114f25420ffTest
https://pubmed.ncbi.nlm.nih.gov/24935680Test

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: Neurosciences [q-bio.NC]. Université Pierre et Marie Curie-Paris VI, 2012. Français. ⟨NNT : 2012PAO66561⟩

مصطلحات موضوعية: cerebral microcirculation, reperfusion régionale, reperfusion injury, ischémie cérébrale focale néonatale, respiration mitochondriale, Neonatal focal cerebral ischemia, Ciclosporine A, pore mitochondrial mPTP, mitochondrial respiration, regional reperfusion, Postconditionnement ischémique, circulation collatérale, microcirculation cérébrale, mitochondrial mPTP pore, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], collateral circulation, ischemic postconditioning, early reperfusion, lésions de la reperfusion, reperfusion précoce

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 inflammatoires de l'ischémie. Néanmoins, la CsA ne réduit pas le volume des lésions cérébrales. Nous avons pu montrer que la Cyclophiline D et le pore mPTP étaient bien deux acteurs majeurs dans la constitution des lésions induites par la reperfusion dans l'ischémie cérébrale focale néonatale. Le postconditionnement ischémique ne permet pas de réduire les volumes des lésions. Nous avons montré que la reperfusion chez le jeune était progressive et lente, sans hyperhémie comme chez l'adulte. Cette cinétique de reperfusion est identique dans les deux hémisphères, tant pour la perfusion tissulaire corticale que pour la perfusion des régions cérébrales profondes. La vasoconstriction cérébrale chez le jeune traduit le recrutement précoce de la circulation collatérale mais aussi les dysfonctionnements de la microcirculation cérébrale. Au final, ces résultats ouvrent la voie à de nouvelles stratégies thérapeutiques spécifiques au profil particulier de la reperfusion dans le cerveau immature

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=od______2592::36680a1eb558efbba0d270c8720fe445Test
https://tel.archives-ouvertes.fr/tel-00833157Test

المؤلفون: S, Benhabbouche, C, Crola da Silva, M, Abrial, R, Ferrera

المصدر: Annales francaises d'anesthesie et de reanimation. 30

مصطلحات موضوعية: Myocardial Stunning, Necrosis, Swine, Coronary Circulation, Ischemic Preconditioning, Myocardial, Animals, Collateral Circulation, Humans, Arrhythmias, Cardiac, Myocardial Reperfusion, Myocardial Reperfusion Injury, Ischemic Postconditioning, Body Temperature

الوصف: The myocardial infarction represents a major cause of mortality. The deleterious phenomena arising during the ischaemia and the reperfusion of the myocardium are studied for more than 40 years. We thought for a long time that the ischaemia was the harmful stage, at the origin of the decrease of the energy stores, the dysregulation of the ionic homeostasis and the metabolic deregulation. We know now that the reperfusion itself is also a source of noxious effects (calcium overload, free radicals production, mitochondrion alteration). To combat these deleterious processes, two maneuvers demonstrated their efficiency by protecting the ischemic myocardium : it is the preconditioning and the postconditionning.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=pmid________::3529944e711bced136743172b0d4180aTest
https://pubmed.ncbi.nlm.nih.gov/21703480Test

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⟩.

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 ...

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