0000000000791053

AUTHOR

W Seeger

showing 2 related works from this author

Simvastatin Inhibits Inflammatory Properties ofStaphylococcus aureusα-Toxin

2002

Background—Simvastatin, a 3-hydroxy-methylglutaryl coenzyme A reductase inhibitor, has been shown to lower serum cholesterol levels in clinical use. Moreover, statins exert beneficial effects in vascular diseases by inhibition of leukocyte rolling, adherence, and transmigration. The aim of this study was to determine if pretreatment with simvastatin attenuatesStaphylococcus aureusα-toxin–induced increase in leukocyte-endothelial interactions during exotoxemia.Methods and Results—The effects of simvastatin on leukocyte-endothelial cell interactions were observed by intravital microscopy in the rat mesenteric microcirculation. Simvastatin (50 or 100 μg/kg) was administered 18 hours before the…

MaleSimvastatinNitric Oxide Synthase Type IIIP-selectinEndotheliumBacterial ToxinsToxemiaInflammationLeukocyte RollingPharmacologyMicrocirculationRats Sprague-DawleyHemolysin ProteinsMesenteric VeinsVenulesCell MovementCulture TechniquesPhysiology (medical)Cell AdhesionLeukocytesmedicineAnimalsMicroscopy Videobusiness.industryAnti-Inflammatory Agents Non-SteroidalHemodynamicsStaphylococcal InfectionsImmunohistochemistryRatsEndothelial stem cellP-Selectinmedicine.anatomical_structureSimvastatinImmunologyEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsNitric Oxide Synthasemedicine.symptomCardiology and Cardiovascular MedicinebusinessIntravital microscopymedicine.drugCirculation
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Staphylococcal α-toxin provokes coronary vasoconstriction and loss in myocardial contractility in perfused rat hearts: Role of thromboxane generation

2000

Background —Cardiac performance is severely depressed in septic shock. Endotoxin has been implicated as the causative agent in Gram-negative sepsis, but similar abnormalities are encountered in Gram-positive sepsis. We investigated the influence of the major exotoxin of Staphylococcus aureus, staphylococcal α-toxin, in isolated perfused rat hearts. Methods and Results —α-Toxin 0.25 to 1 μg/mL caused a dose-dependent increase in coronary perfusion pressure that more than doubled. In parallel, we noted a decrease in left ventricular developed pressure and the maximum rate of left ventricular pressure rise (dP/dt max ), dropping to a minimum of <60% of control. These changes were accompani…

MaleThromboxaneIndomethacinProstacyclinVentricular Function LeftHemolysin ProteinsThromboxane A2chemistry.chemical_compoundEdemaPhenylacetatesSulfonamidesHeartAzepinesPerfusionAnesthesiaLactatesVentricular pressuremedicine.symptomCardiology and Cardiovascular Medicinemedicine.drugStaphylococcus aureusmedicine.medical_specialtyBacterial ToxinsExotoxinsIn Vitro TechniquesSepsisContractilityThromboxane A2Physiology (medical)Internal medicinemedicineAnimalsMasoprocolPlatelet Activating FactorRats WistarAspirinL-Lactate Dehydrogenasebusiness.industryTriazolesmedicine.diseaseEpoprostenolMyocardial ContractionRatsEndocrinologychemistryVasoconstrictionPotassiumCoronary perfusion pressurebusinessPlatelet Aggregation InhibitorsVasoconstriction
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