15 research outputs found

    Préconditionnement et postconditionnement myocardiques induits par les agents anesthésiques halogénés

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    Volatile anesthetics protect myocardium against reversible and irreversible ischemic injury. Using a rabbit in vivo model, we compared the potency of four different halogenated to induce preconditioning. We shown that brain death induced catecholamines storm retains the ability to protect the heart by isoflurane inhalation. A new emulsified formulation of halogenated administered intravenously induces acute and delayed preconditioning. Mitochondrial adenosine triphosphate-sensitive potassium channels and mechanogated channels are involved in halogenated-induced acute preconditioning. Desflurane-induced preconditioning improved the resistance of the mitochondrial permeability transition pore to calcium-induced opening. Endothelial nitric oxide synthase is a trigger and mediator of delayed preconditioning by isoflurane. Isoflurane acts during early reperfusion by activation of the phosphatidylinositol-3-kinase signallingLes agents anesthésiques halogénés peuvent induire un préconditionnement myocardique. A partir d un modÚle expérimental de lapin in vivo, nous avons comparé les effets protecteurs des différents halogénés et démontré par ailleurs la persistance de ce préconditionnement aprÚs mort encéphalique. Une nouvelle formulation de ces agents anesthésiques, présentés en émulsion lipidique, induit un préconditionnement précoce et tardif aprÚs administration intra-veineuse. Le préconditionnement précoce met en jeu l ouverture des canaux potassiques ATP dépendants mitochondriaux ainsi que les canaux stretch et se traduit par un retard à l ouverture du pore de transition de perméabilité mitochondriale induit par une surcharge calcique. Les halogénés induisent un préconditionnement tardif dont la signalisation passe par le monoxyde d azote. Ces agents sont enfin capables d induire un postconditionnement lorsqu ils sont administrés dÚs les premiers instants de la reperfusion myocardiqueLYON1-BU.Sciences (692662101) / SudocSudocFranceF

    Cyclophilin D modulates the cardiac mitochondrial target of isoflurane, sevoflurane, and desflurane

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    Background: Volatile anesthetics are known to limit myocardial ischemia-reperfusion injuries. Mitochondria were shown to be major contributors to cardioprotection. Cyclophilin D (CypD) is one of the main regulators of mitochondria-induced cell death. We compared the effect of isoflurane, sevoflurane, and desflurane in the presence or absence of CypD, to clarify its role in the mechanism of cardioprotection induced by these anesthetics.Methods: Oxidative phosphorylation, mitochondrial membrane potential, and H2O2 production were measured in isolated mitochondria from wild-type (WT) or CypD knockout mice in basal conditions and after hypoxia-reoxygenation in the presence or absence of volatile anesthetics.Results: All volatile anesthetics inhibited mitochondrial state 3 of complex I, decreased membrane potential, and increased adenosine diphosphate consumption duration in both WT and CypD knockout mice. However, they differently modified H2O2 production after stimulation by succinate: CypD ablation reduced H2O2 production, isoflurane decreased H2O2 level in WT but not in CypD knockout mice, sevoflurane affected both lines whereas desflurane increased H2O2 production in CypD knockout and had no effect on WT mice.Conclusions: This study showed different effects of isoflurane, sevoflurane, and desflurane on mitochondrial functions and highlighted the implication of CypD in the regulation of adenosine diphosphate consumption and complex I-induced radical oxygen species production

    A modified calcium retention capacity assay clarifies the roles of extra- and intracellular calcium pools in mitochondrial permeability transition pore opening

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    International audienceThe abbreviations used are: SERCA, sarco/endoplasmic Ca 2Ï© ATPase; CRC, Ca 2Ï© retention capacity; AR, anoxia-reoxygenation; mPTP, mitochondria permeability transition pore; CsA, cyclosporine A; CypD, cyclophilin D; CICR, Ca 2Ï©-induced Ca 2Ï© release; FCCP, carbonyl cyanide p-trifluoromethoxyphenylhydrazone; A.U., arbitrary unit(s); ANOVA, analysis of variance. cro tapraid4/zbc-bc/zbc-bc/zbc99919/zbc1234-19z ZSUBMIT 11 xppws SÏ­3 10/9/19 4:07 4/Color Figure(s) F1-

    Tetranuclear copper(II) complexes with macrocyclic and open-chain disiloxane ligands as catalyst precursors for hydrocarboxylation and oxidation of alkanes and 1-phenylethanol

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    Two new tetranuclear complexes [Cu-4(mu-O)(L-1)-Cl-4] and [Cu-4(mu(4)-O)(L-2)(2)Cl-4] (2), where H2L1 is a macrocyclic ligand resulting from [2+2] condensation of 2,6-diformy1-4-methylphanol (DFF) and 1,3-bis(aminopropy1)tetramethyldisiloxane, and HL2 is a 1:2 condensation product: of DFF with trimethylsilyl p-aminobenzoate, have been prepared. The structures of the products were established by Xray diffraction. The complexes have been characterised by FTIR, UV/Vis spectroscopy, ES1 mass-spectrometry and magnetic susceptibility measurements. The latter revealed that the letrftriuclear complexes can be descr bed as two ferromagnetically coupled dinuclear units, in which the two copper(II) ions interact antiferromacinetically. The ccimpi.iunds act as homogeneous catalyst precursors for a number of single-pot reactions, including (I) hydrocarbaxylation, with CO, H2O and K2S2O8, of a variety of linear and cyclic (n = 5-8) alkanes into the corresponding Cn+1 carboxylic acids, (ii) peroxidative oxidation of cyclohexane, and (iii) solvent-free microwave-assisted oxidation of 1-phenyletha.nol
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