Search results for "Perfusion"

showing 10 items of 714 documents

Hepatic metabolism of diallyl disulfide in rat and man

2003

International audience; 1. The metabolism of diallyl disulphide was investigated in vitro with rat and human liver cell subfractions and ex vivo with an isolated perfused rat liver. 2. Diallyl disulphide was oxidized to diallylthiosulphinate by rat liver microsomes with an apparent K-m = 0.86 +/- 0.1 mM and an apparent V-max = 0.47 +/- 0.12 nmol min(-1) mg(-1) protein (mean +/- SE). Both cytochrome P450 (CYP) and flavin-containing monooxygenases were involved, with CYP2B1/2 and CYP2E1 being the most active CYP enzymes. 3. In rat and man, microsomal oxidation of allylmethyl sulphide to allylmethyl sulphoxide and allylmethyl sulphone also occurred, although at a low rate. Diallyl disulphide w…

MaleLIVERHealth Toxicology and MutagenesisToxicologyBiochemistryGARLICchemistry.chemical_compoundDisulfides0303 health sciencesbiologyDADS030302 biochemistry & molecular biologyCytochrome P-450 CYP2E1General MedicineCYP2E1Middle Agedfoie3. Good healthEnzymesAllyl CompoundsPerfusionBiochemistryArea Under CurveMicrosomes LiverFemaleAryl Hydrocarbon HydroxylasesOxidation-Reductionailcomposé soufrexénobiotique[SDV.BID]Life Sciences [q-bio]/BiodiversityIn Vitro Techniques03 medical and health sciencesAnimalsHumansmétabolisme030304 developmental biologyAgedPharmacologySulfur CompoundsEX VIVOCytochrome P450SULFUR COMPOUNDMetabolismGlutathioneMonooxygenaseRatschemistryDADS;EX VIVO;SULFUR COMPOUND;XENOBIOTIC METABOLISM;GARLIC;LIVER;RATCytochrome P-450 CYP2B1Steroid HydroxylasesMicrosomebiology.proteinRATAllyl MercaptanXENOBIOTIC METABOLISMDrug metabolism
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Endothelial kinin B1‐receptors are induced by myocardial ischaemia‐reperfusion in the rabbit

2001

Kinin B1-receptors are induced by various inflammatory stimuli. Since myocardial ischaemia-reperfusion results in inflammation, we questioned whether it could induce B1-receptor-dependent responses to des-Arg9-bradykinin (DBK). Thirty-six rabbits were submitted either to a 30 min coronary occlusion followed by a 3 h reperfusion or to a sham operation. The response to DBK was then tested in vivo on mean arterial pressure (MAP) and in vitro on isolated hearts and arterial rings. DBK induced a dose-dependent decrease in MAP in the ischaemia-reperfusion group (DBK, 10 μg kg−1, intra-arterial: -12 ± 2 vs. -5 ± 2 mmHg in the sham group, P < 0.02), which was significantly antagonised by [Leu8]-des…

MaleMean arterial pressuremedicine.medical_specialtyEndotheliumPhysiologyBlotting WesternBradykininBlood PressureMyocardial Reperfusion InjuryInflammationIn Vitro TechniquesBradykininReceptor Bradykinin B1Muscle Smooth Vascularchemistry.chemical_compoundIsometric ContractionInternal medicinemedicineAnimalsMesenteric arteriesDose-Response Relationship Drugbiologybusiness.industryReceptors BradykininAngiotensin-converting enzymeOriginal ArticlesKininImmunohistochemistryMyocardial ContractionPerfusionmedicine.anatomical_structureEndocrinologychemistryImmunologybiology.proteinCoronary perfusion pressureEndothelium VascularRabbitsmedicine.symptombusinessThe Journal of Physiology
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Prospective Study on Functional Results After Lung-Sparing Radical Pleurectomy in the Management of Malignant Pleural Mesothelioma

2012

Introduction:Malignant pleural mesothelioma (MPM) can reduce lung function by entrapping lung parenchyma via a rind of tumor with or without concurrent effusion. Radical pleurectomy (RP) allows expansion of the trapped lung. The purpose of this study was to investigate changes in pulmonary function and lung perfusion in patients undergoing RP.Methods:In a prospective, nonrandomized study, all patients with histologically proven MPM were evaluated from January to December 2010 for trimodality therapy including RP as surgical procedure. Pulmonary-function tests and perfusion scans were obtained before and 2 months after RP. Primary end points were pulmonary function (forced vital capacity [FV…

MaleMesotheliomaPulmonary and Respiratory MedicineVital capacitymedicine.medical_specialtyPulmonary functionPleural Neoplasmsmedicine.medical_treatmentVital CapacityUrologyPulmonary function testingFEV1/FVC ratiomedicineHumansProspective StudiesMesotheliomaDecorticationProspective cohort studyPleurectomyAgedLungbusiness.industryrespiratory systemDecorticationPrognosismedicine.diseaseRespiratory Function Testsrespiratory tract diseasesSurgeryPerfusionmedicine.anatomical_structureOncologyEffusionFemalebusinessJournal of Thoracic Oncology
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Low-Flow Desflurane and Sevoflurane Anesthesia Minimally Affect Hepatic Integrity and Function in Elderly Patients: Retracted

2000

UNLABELLED Hepatic blood flow is reduced in a dose-related manner by all inhaled anesthetics now in use. We assessed hepatic function in elderly patients anesthetized with desflurane or sevoflurane. We measured the cytosolic liver enzyme alpha glutathione S-transferase (alpha GST), the formation of the lidocaine metabolite monoethylglycinexylidide (MEGX), and gastric mucosal tonometry-derived variables as sensitive markers of hepatic function and splanchnic perfusion. Thirty patients, 70 to 90 yr old, were allocated randomly to receive desflurane or sevoflurane anesthesia. Anesthetic exposure ranged from 2.1-4.5 minimum alveolar concentration hours. No significant changes in standard liver …

MaleMethyl EthersMinimum alveolar concentrationLidocaineSevofluraneSevofluraneDesfluranemedicineHumansAgedGlutathione TransferaseAged 80 and overIsofluranebusiness.industryLidocaineAnesthesiology and Pain MedicineLiverGastric MucosaAnesthesiaAnesthetics InhalationAnestheticFemaleLiver functionSplanchnicbusinessDesfluranePerfusionmedicine.drugAnesthesia &amp; Analgesia
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The Long-Term Effect of Sevoflurane on Neuronal Cell Damage and Expression of Apoptotic Factors After Cerebral Ischemia and Reperfusion in Rats

2006

We investigated the long-term effects of sevoflurane on histopathologic injury and key proteins of apoptosis in a rat hemispheric ischemia/reperfusion model. Sixty-four male Sprague-Dawley rats were randomly assigned to Group 1 (fentanyl and N2O/O2; control) and Group 2 (2.0 vol% sevoflurane and O2/air). Ischemia (45 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure 40 mm Hg). Animals were killed after 1, 3, 7, and 28 days. In hematoxylin and eosin-stained brain sections eosinophilic hippocampal neurons were counted. Activated caspase-3 and the apoptosis-regulating proteins Bax, Bcl-2, Mdm-2, and p53 were analyzed by i…

MaleMethyl Ethersmedicine.medical_specialtyH&E stainIschemiaCell CountHippocampal formationHippocampusNeuroprotectionSevofluraneBrain IschemiaRats Sprague-DawleySevofluraneInternal medicineEosinophilicmedicineAnimalsNeuronsCaspase 3business.industrymedicine.diseaseImmunohistochemistryRatsEnzyme ActivationNeuroprotective AgentsAnesthesiology and Pain MedicineBlood pressureEndocrinologyCaspasesCerebrovascular CirculationReperfusion InjuryAnesthesiaAnesthetics InhalationApoptosis Regulatory ProteinsbusinessBlood Flow VelocityImmunostainingmedicine.drugAnesthesia &amp; Analgesia
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Dynamic in vivo Imaging of Microvasculature and Perfusion by Miniaturized Confocal Laser Microscopy

2008

&lt;i&gt;Introduction:&lt;/i&gt; Microvasculature and associated pathologies mandate dynamic imaging. We evaluated a novel miniaturized confocal laser scanning probe for in vivo visualization of blood vessels, blood flow, cell tracking and perfusion in both healthy rodents and disease models.&lt;i&gt; Methods:&lt;/i&gt; The hand-held confocal microscopy system allowed a 500- to 2,400-fold magnification at a dynamically variable imaging depth. Different intravital stains were used alone or in combination for tissue, nuclear, plasma and vascular endothelial cell staining and for blood flow visualization, and targeted staining for individual cell populations. &lt;i&gt;Results:&lt;/i&gt; Precis…

MaleMice Inbred MRL lprPathologymedicine.medical_specialtyMaterials scienceLaser scanningDynamic imagingConfocalCell Communicationlaw.inventionMiceImaging Three-DimensionalIn vivoConfocal microscopylawMicroscopyLeukocytesmedicineAnimalsFluorescent DyesInflammationMicroscopy ConfocalMiniaturizationMicrocirculationBrainEndothelial CellsThrombosisLupus NephritisMice Inbred C57BLDisease Models AnimalMicrovesselsFemaleSurgeryIntracranial ThrombosisGerbillinaePerfusionBlood Flow VelocityPreclinical imagingBiomedical engineeringEuropean Surgical Research
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Genomic response of the rat brain to global ischemia and reperfusion

2008

To identify genes that are involved in ischemia response of the brain, we have evaluated changes of gene expression in rat cerebrum after 15 min complete global ischemia, followed by reperfusion for 1 h, 6 h or 24 h. The expression profiles of approximately 30,000 transcripts from three subjects in each group (including sham-operated controls) were monitored employing oligonucleotide microarrays. About 20,000 transcripts were detectable in rat brains. The levels of 576 transcripts (approximately 2.9%) were significantly altered in response to experimental ischemia. 419 transcripts were up- and 157 downregulated; 39 transcripts changed after 1 h reperfusion, 174 after 6 h and 462 after 24 h.…

MaleMicroarrayIschemiaBiologyBrain IschemiaGene expressionmedicineAnimalsCluster AnalysisRats WistarMolecular BiologyOligonucleotide Array Sequence AnalysisRegulation of gene expressionReverse Transcriptase Polymerase Chain ReactionMicroarray analysis techniquesGene Expression ProfilingGeneral NeuroscienceBrainmedicine.diseaseMolecular biologyRatsGene expression profilingReverse transcription polymerase chain reactionReal-time polymerase chain reactionGene Expression RegulationReperfusionRNANeurology (clinical)Developmental BiologyBrain Research
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Aspirin protects striatal dopaminergic neurons from neurotoxin-induced degeneration: an in vivo microdialysis study.

2006

The effect of aspirin on dopaminergic neuronal damage induced by in vivo infusion of 1-methyl-4-phenylpiridinium iodide (MPP(+)) and 6-hydroxydopamine (6-OHDA) was studied in rats, using microdialysis. Rat striata were perfused with 1 mM MPP(+) or 6-OHDA for 10 min, causing peak levels of dopamine (DA) in the dialytic fluid, after 40 min. After 24 h, 1 mM MPP(+) was perfused again for 10 min and DA levels measured in the dialytic fluid, as an index of neuronal cell integrity. Pretreatment with Aspidol (lysine acetylsalicylate), 180 mg/kg i.p., 1 h before MPP(+) or 6-OHDA perfusion, did not modify DA extracellular output, on day 1, but restored MPP(+)-induced DA release on day 2, indicating …

MaleMicrodialysisTyrosine 3-MonooxygenaseDopamineMicrodialysisNeurotoxinsPharmacologyNeuroprotectionSettore BIO/09 - FisiologiaRats Sprague-Dawleychemistry.chemical_compoundIn vivoHydroxybenzoatesNeurotoxinAnimalsDrug InteractionsMolecular BiologyChromatography High Pressure LiquidNeuronsAnalysis of VarianceAspirinGeneral NeuroscienceMPTPDopaminergicImmunohistochemistryCorpus StriatumRatsNeuroprotective Agentsnervous systemchemistryAnesthesiaNerve DegenerationNeurology (clinical)Aspirin in vivo microdialysisPerfusionOxidopamineDevelopmental Biology
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Preconditioning by Mitochondrial Reactive Oxygen Species Improves the Proangiogenic Potential of Adipose-Derived Cells-Based Therapy

2009

Objective— Transplantation of adipose-derived stroma cells (ADSCs) stimulates neovascularization after experimental ischemic injury. ADSC proangiogenic potential is likely mediated by their ability to differentiate into endothelial cells and produce a wide array of angiogenic and antiapoptotic factors. Mitochondrial reactive oxygen species (ROS) have been shown to control ADSC differentiation. We therefore hypothesized that mitochondrial ROS production may change the ADSC proangiogenic properties. Methods and Results— The use of pharmacological strategies (mitochondrial inhibitors, antimycin, and rotenone, with or without antioxidants) allowed us to specifically and precisely modulate mito…

MaleMitochondrial ROSProgrammed cell deathStromal Cells/cytology/metabolismAngiogenesisCellsReactive Oxygen Species/*metabolismNeovascularization PhysiologicBiologyMitochondrionmedicine.disease_causeMice03 medical and health sciences0302 clinical medicineAdipocytesmedicineAnimalsEndothelial Cells/*cytology/*physiologyCells CulturedNeovascularization030304 developmental biologyMitochondria/*metabolismchemistry.chemical_classificationReperfusion Injury/physiopathology0303 health sciencesReactive oxygen speciesCulturedEndothelial CellsCell DifferentiationMitochondriaCell biologyCell Differentiation/*physiologyTransplantationPhysiologic/*physiologychemistryReperfusion Injury030220 oncology & carcinogenesisImmunologyStromal CellsStem cellReactive Oxygen SpeciesCardiology and Cardiovascular MedicineOxidative stressArteriosclerosis, Thrombosis, and Vascular Biology
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Novel Small Molecule Inhibitor of C1s Exerts Cardioprotective Effects in Ischemia-Reperfusion Injury in Rabbits

2001

Abstract Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic agents, adhesion molecule expression, release of cytokines and oxygen-derived free radicals, and subsequent neutrophil accumulation. In the present study the cardioprotective effects of a novel highly selective small molecule C1s inhibitor (C1s-INH-248, Knoll) were examined in a rabbit model of myocardial ischemia (I) and reperfusion (R; i.e., 60 min I + 180 min R). In in vitro tests (enzyme activity and SRBC lysis) C1s-INH-248 demonstrated profound inhibitory potency. In vivo C1s-INH-248 (1 mg/kg body weight) administered 5 min before reperfusion significantly attenuated m…

MaleNecrosisEndotheliumNeutrophilsG proteinImmunologyMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryComplement C1 Inactivator ProteinsPharmacologyHemolysisLeukocyte CountClassical complement pathwaySuperoxidesIn vivomedicineAnimalsImmunology and AllergyComplement Activationbusiness.industryHemodynamicsmedicine.diseaseComplement systemmedicine.anatomical_structureAnesthesiaEndothelium VascularRabbitsmedicine.symptombusinessReperfusion injuryThe Journal of Immunology
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