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Titolo:
Biosynthesis of constitutive nitric oxide synthase-derived nitric oxide attenuates coronary vasoconstriction and myocardial depression in a model of septic heart failure induced by Staphylococcus aureus alpha-toxin
Autore:
Grandel, U; Sibelius, U; Schrickel, J; Schmidt, D; Buerke, M; Fink, L; Bournelis, E; Heep, M; Mayer, K; Bohle, RM; Seeger, W; Grimminger, F;
Indirizzi:
Univ Giessen, Dept Internal Med, D-35392 Giessen, Germany Univ Giessen Giessen Germany D-35392 ernal Med, D-35392 Giessen, Germany Univ Mainz, Dept Internal Med, D-6500 Mainz, Germany Univ Mainz Mainz Germany D-6500 Dept Internal Med, D-6500 Mainz, Germany Univ Giessen, Dept Pathol, Giessen, Germany Univ Giessen Giessen Germany niv Giessen, Dept Pathol, Giessen, Germany
Titolo Testata:
CRITICAL CARE MEDICINE
fascicolo: 1, volume: 29, anno: 2001,
pagine: 1 - 7
SICI:
0090-3493(200101)29:1<1:BOCNOS>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; RIGHT VENTRICULAR DYSFUNCTION; ISOLATED-PERFUSED HEART; BACTERIAL EXOTOXINS; EJECTION FRACTION; CARDIAC MYOCYTE; RABBIT LUNGS; SHOCK; RELEASE; CIRCULATION;
Keywords:
heart failure; shock; septic; Staphylococcus aureus; exotoxins; coronary circulation; nitric oxide; nitric oxide synthase; polymerase chain reaction; immunohistochemistry; chemiluminescence;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Grimminger, F Univ Giessen, Dept Internal Med, Klin Str 36, D-35392 Giessen, Germany Univ Giessen Klin Str 36 Giessen Germany D-35392 n, Germany
Citazione:
U. Grandel et al., "Biosynthesis of constitutive nitric oxide synthase-derived nitric oxide attenuates coronary vasoconstriction and myocardial depression in a model of septic heart failure induced by Staphylococcus aureus alpha-toxin", CRIT CARE M, 29(1), 2001, pp. 1-7

Abstract

Objective: Myocardial depression, which frequently occurs in the course ofseptic shock, has been attributed to the cardiodepressant properties of nitric oxide (NO) generated by either the inducible NO synthase (iNOS) or theconstitutive isoform (cNOS). We have previously demonstrated that alpha -toxin from Staphylococcus aureus induces thromboxane-mediated vasoconstriction accompanied by severe cardiodepression in isolated rat hearts. In the present study, we investigated the role of NO in the alpha -toxin-induced vascular and contractile abnormalities. Design: Prospective, experimental study. Setting: Research laboratory at a university hospital. Subjects: Isolated hearts from male Wistar rats. Interventions: Isolated hearts were perfused with purified staphylococcal alpha -toxin for 60 mins. Measurements and Main Results: At a concentration of 0.25 and 0.5 mug/mL, alpha -toxin induced a rise in coronary perfusion pressure, depressed myocardial contractility, and caused edema formation. Simultaneously, a time- and dose-dependent rapid release of NO into the perfusate was noted as quantified by a chemiluminescence technique. L-NMMA, a nonselective inhibitor of NOS, but not PBITU, an iNOS-selective inhibitor, blocked NO synthesis, markedly increased the rise in coronary perfusion pressure and the loss in contractility, and enhanced edema formation in response to alpha -toxin. In contrast, zaprinast, a selective inhibitor of phosphodiesterase type V that isused for stabilization of cyclic guanosine monophosphate, attenuated the toxin-induced coronary vasoconstrictor response and the myocardial depression. L-arginine, the substrate of NOS, had similar, yet less potent, effects as zaprinast and slightly increased the release of NO caused by alpha -toxin. Immunohistochemical analysis of the myocardium at the end of the perfusion period demonstrated a positive staining for cNOS but not for iNOS. In addition, no up-regulation of iNOS mRNA was detected in the tissue of toxin-exposed hearts. Conclusions: Staphylococcal alpha -toxin provokes NO biosynthesis via activation of cNOS in rat hearts. MO partly antagonizes the deleterious effectsof this pathogenicity factor on coronary vasoregulation and myocardial performance.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 13:14:42