CCL

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1.

001-es BibID:BIBFORM040581
Első szerző:Bódi Annamária (kardiológus)
Cím:The cardiotonic effects of levosimendan in guinea pig hearts are modulated by beta-adrenergic stimulation / Bódi A., Szilágyi Sz., Édes I., Papp Z.
Dátum:2003
Megjegyzések:The effects of the Ca2+-sensitiser levosimendan alone or in combination with beta-adrenergic stimulation on the contractile function were studied in various guinea pig cardiac preparations. Echocardiography in narcotised animals indicated that a maximal dose of levosimendan (50 microg x kg(-1)) increased the left ventricular posterior wall movement velocity during systoles and diastoles by 25 +/- 3% (mean +/- S.E.M.) and 17 +/- 2%, respectively. In Langendorff hearts, a saturating concentration of levosimendan (0.3 micromol x l(-1) for 5 min) increased +dP/dt(max) and dP/dt(max) by 28 +/- 3% and 14 +/- 2%, respectively. Further, the Ca2+-sensitising potential of levosimendan in Triton-skinned cardiomyocytes (EC50: 5 +/- 3 nmol x l(-1)) was illustrated by a maximal increase in the isometric force production by 51 +/- 5% (at pCa 6.2). However, following stimulation by isoproterenol, when the level of troponin I phosphorylation was elevated, no significant additional increase in the contractile parameters could be demonstrated upon levosimendan administration. Moreover, the levosimendan-induced increase in force production in isolated skinned myocytes could be prevented by incubation with the catalytic subunit of protein kinase A (100 U x ml(-1) for 40 min). These data indicate that thin filament-targeted Ca2+-sensitisation by levosimendan is modulated by phosphorylation of the contractile filaments, an effect that should be considered during combination therapy with levosimendan.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:General Physiology and Biophysics. - 22 : 3 (2003), p. 313-327. -
További szerzők:Szilágyi Szabolcs (1976-) (kardiológus) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:T 035279
OTKA
NKFP 1/007/2001
Egyéb
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2.

001-es BibID:BIBFORM040636
Első szerző:Kristóf Éva (kardiológus)
Cím:The effects of levosimendan on the left ventricular function and protein phosphorylation in post-isschemic guinea pig hearts / Kristof, E., Szigeti, G., Papp, Z., Bodi, A., Ball, N. A., Walsh, R. A., Edes, I.
Dátum:1999
ISSN:0300-8428
Megjegyzések:The widely accepted theories for the decreased function in the stunned myocardium relate to Ca2+ desensitization and free radical-mediated tissue damage of the myofilaments. The aim of the present study was to examine whether the depressed contractile function and Ca2+ responsiveness of the stunned myocardium may be restored by a new Ca2+ sensitizer (levosimendan), which has been shown to improve the Ca2+ response of the myofilaments. The effects of levosimendan on the left ventricular function and the in vivo protein phosphorylation were examined in both the non-ischemic and the stunned myocardium. Myocardial stunning was induced in Langendorff-perfused guinea pig hearts by suspending the circulation for 8 min, followed by a 20-min reperfusion period. Perfusion of post-ischemic guinea pig hearts with levosimendan (0.03?0.48 ?M, 6 min) was associated with dose- and time-dependent increases in both dP/dtmax (contractility) and dP/dtmin (speed of relaxation). When the effectiveness of levosimendan was compared in non-ischemic and post-ischemic hearts, no significant differences were noted in the relative stimulatory effects on contractility and relaxation, at any given time point (time-response curve) or concentration (dose-response curve). Perfusion of the guinea pig hearts with a high (0.3 ?M) levosimendan concentration did not reveal any qualitative or quantitative difference in the phosphodiesterase inhibitory potential of the compound (elevation of tissue cyclic AMP levels and characteristics of protein phosphorylation) between the non-ischemic and the post-ischemic myocardium. However, when isoproterenol was adminstered to induce maximal in vivo phosphorylation of cardiac phosphorproteins, an attenuation of the 32P-incorporation into troponin I was noted in the post-ischemic hearts. The decrease in isoproterenol-induced 32P-incorporation into troponin I was associated with similar alterations in the tissue level of this protein. We conclude that the Ca2+ sensitizer levosimendan exerts dose- and time-dependent positive inotropic and lusitropic effects on the postischemic myocardium, lending support to the hypothesis tha Ca2+ desensitization of the myofibrils is involved in myocardial stunning.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Calcium sensitizers
cAMP
desensitization
myocardial ischemia
protein phosphorylation
Megjelenés:Basic Research In Cardiology. - 94 : 4 (1999), p. 223-230. -
További szerzők:Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Papp Zoltán (1965-) (kardiológus, élettanász) Bódi Annamária (1957-) (kardiológus) Ball, N. A. Walsh, R. A. Édes István (1952-) (kardiológus)
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3.

001-es BibID:BIBFORM040611
Első szerző:Kristóf Éva (kardiológus)
Cím:Cardiac responses to calcium sensitizers and isoproterenol in intact guinea pig hearts : effects on cyclic AMP levels, protein phosporylation, myoplasmic calcium concentration and left ventricular function / Kristóf É., Szigeti Gy., Papp Z., Bódi Á., Facskó A., Kovács L., Papp J. G., Kranias, E.G., Édes I.
Dátum:1998
ISSN:0077-8923
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Annals Of The New York Academy Of Sciences. - 853 : 1 (1998), p. 316-319. -
További szerzők:Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Papp Zoltán (1965-) (kardiológus, élettanász) Bódi Annamária (1957-) (kardiológus) Facskó Andrea (1953-) (szemész) Kovács László (1939-) (élettanász) Papp Gy. Julius (Szeged) Kranias, Evangelia G. Édes István (1952-) (kardiológus)
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