0000000000811843

AUTHOR

Ladislau Kiss

showing 2 related works from this author

Staphylococcal alpha-toxin provokes neutrophil-dependent cardiac dysfunction: role of ICAM-1 and cys-leukotrienes.

2002

The role of polymorphonuclear neutrophils (PMN) in septic myocardial dysfunction is presently unknown. Staphylococcus aureus infections are frequently associated with septic sequelae. Therefore, we perfused isolated rat hearts with low doses of α-toxin, the major staphylococcal exotoxin, followed by application of human PMN, N-formyl-methionyl-leucyl-phenylalanine, and arachidonic acid. In contrast to sham-perfused hearts (no α-toxin), a rise in coronary perfusion pressure (CPP) and a reduction of contractile function were noted, and cardiac expression of intercellular adhesion molecule (ICAM)-1 was detected by immunohistochemical methods and real-time PCR. Histological analysis and myelope…

LeukotrienesHeart diseasePhysiologyNeutrophilsNeutrophileBacterial ToxinsExotoxinsThiophenesIn Vitro Techniquesmedicine.disease_causePathogenesisHemolysin ProteinsPhysiology (medical)medicineAnimalsHumansICAM-1Arachidonic AcidToxinbusiness.industryMyocardiumHydrazonesHeartmedicine.diseaseIntercellular Adhesion Molecule-1RatsN-Formylmethionine Leucyl-PhenylalaninePerfusionStaphylococcus aureusImmunologyCirculatory systemCardiology and Cardiovascular MedicinebusinessOligonucleotide ProbesExotoxinAmerican journal of physiology. Heart and circulatory physiology
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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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