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1.

001-es BibID:BIBFORM016600
Első szerző:Bárándi László (élettanász)
Cím:Reverse rate-dependent changes are determined by baseline action potential duration in mammalian and human ventricular preparations / Bárándi László, Virág László, Jost Norbert, Horváth Zoltán, Koncz István, Papp Rita, Harmati Gábor, Horváth Balázs, Szentandrássy Norbert, Bányász Tamás, Magyar János, Zaza Antonio, Varró András, Nánási Péter P.
Dátum:2010
ISSN:0300-8428
Megjegyzések:Class III antiarrhythmic agents exhibit reverse rate-dependent lengthening of the action potential duration (APD). In spite of the several theories developed so far to explain this reverse rate-dependency (RRD), its mechanism has not yet been clarified. The aim of the present work was to further elucidate the mechanisms responsible for RRD in mammalian ventricular myocardium. Action potentials were recorded using conventional sharp microelectrodes from human, canine, rabbit and guinea pig ventricular myocardium in a rate-dependent manner varying the cycle length (CL) between 0.3 and 5 s. Rate-dependent drug effects were studied using agents known to lengthen or shorten action potentials, and these drug-induced changes in APD were correlated with baseline APD values. Both drug-induced lengthening (by dofetilide, sotalol, E-4031, BaCl2, veratrine, BAY K 8644) and shortening (by mexiletine, tetrodotoxin, lemakalim) of action potentials displayed RRD, i.e., changes in APD were greater at longer than at shorter CLs. In rabbit, where APD is a biphasic function of CL, the drug-induced APD changes were proportional to baseline APD values but not to CL. Similar results were obtained when repolarization was modified by injection of inward or outward current pulses in isolated canine cardiomyocytes. In each case the change in APD was proportional to baseline APD (i.e., that measured before the superfusion of drug or injection of current). Also, the net membrane current (Inet), determined from the action potential waveform at the middle of the plateau, was inversely proportional to APD and consequently with to CL. The results indicate that RRD is a common characteristic of all the drugs tested regardless of the modified ion current species. Thus, drug-induced RRD can be considered as an intrinsic property of cardiac membranes based on the inverse relationship between Inet and APD.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Ventricular repolarization
Action potential duration
Reverse rate dependence
Membrane current
Human myocardium
Mammalian cardiac cells
egyetemen (Magyarországon) készült közlemény
Megjelenés:Basic Research In Cardiology. - 105 : 3 (2010), p. 315-323. -
További szerzők:Virág László (élettanász Szeged) Jost Norbert Horváth Zoltán Koncz István (Szeged) Papp Rita Harmati Gábor (1983-) (élettanász) Horváth Balázs (1981-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Zaza, Antonio Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM030699
Első szerző:Czuriga Dániel (kardiológus)
Cím:Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure / Czuriga Dániel, Tóth Attila, Pásztor Enikő T., Balogh Ágnes, Bodnár Andrea, Nizsalóczki Enikő, Lionetti Vincenzo, Recchia Fabio A., Czuriga István, Édes István, Papp Zoltán
Dátum:2012
ISSN:0300-8428
Megjegyzések:We tested the hypothesis that myocardial contractile protein phosphorylation and the Ca2+ sensitivity of force production are dysregulated in a porcine model of pacing-induced heart failure (HF). The level of protein kinase A (PKA)-dependent cardiac troponin I (TnI) phosphorylation was lower in the myocardium surrounding the pacing electrode (pacing site) of the failing left ventricle (LV) than in the controls. Immunohistochemical assays of the LV pacing site pointed to isolated clusters of cardiomyocytes exhibiting a reduced level of phosphorylated TnI. Flow cytometry on isolated and permeabilized cardiomyocytes revealed a significantly larger cell-to-cell variation in the level of TnI phosphorylation of the LV pacing site than in the opposite region in HF or in either region in the controls: the interquartile range (IQR) on the distribution histogram of relative TnI phosphorylation waswider at the pacing site (IQR = 0.53) than that at the remote site of HF (IQR = 0.42; P = 0.0047) or that of the free wall of the control animals (IQR = 0.36; P = 0.0093). Additionally, the Ca2+ sensitivities of isometric force production were higher and appeared to be more variable in single permeabilized cardiomyocytes from the HF pacing site than in the healthy myocardium. In conclusion, the level of PKA-dependent TnI phosphorylation and the Ca2+ sensitivity of force production exhibited a high cell-to-cell variability at the LV pacing site, possibly explaining the abnormalities of the regional myocardial contractile function in a porcine model of pacing-induced HF.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Egészség- és Környezettudomány
Cardiac function
Pacing-induced heart failure
Beta-adrenergic signaling
Dilated cardiomyopathy
Cardiac troponin I
Megjelenés:Basic Research In Cardiology. - 107 : 2 (2012), p. 1-13. -
További szerzők:Tóth Attila (1971-) (biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Balogh Ágnes (1984-) (kardiológus) Dóczy-Bodnár Andrea (1970-) (biofizikus) Nizsalóczki Enikő Lionetti, Vincenzo Recchia, Fabio A. Czuriga István (1948-2018) (kardiológus) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vascularis rizikó- és stroke betegek vizsgálata
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Membrán dinamika
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM094562
035-os BibID:(cikkazonosító)24 (WoS)000639453800001 (Scopus)85104214308 (PubMed)33844095
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Omecamtiv mecarbil evokes diastolic dysfunction and leads to periodic electromechanical alternans / Fülöp Gábor Á., Oláh Attila, Csipo Tamas, Kovács Árpád, Pórszász Róbert, Veress Roland, Horváth Balázs, Nagy László, Bódi Beáta, Fagyas Miklós, Helgadottir Solveig Lind, Bánhegyi Viktor, Juhász Béla, Bombicz Mariann, Priksz Daniel, Nanasi Peter, Merkely Béla, Édes István, Csanádi Zoltán, Papp Zoltán, Radovits Tamás, Tóth Attila
Dátum:2021
ISSN:0300-8428
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Basic Research In Cardiology. - 116 : 1 (2021), p. 24. -
További szerzők:Oláh Attila (sebész) Csípő Tamás (1990-) Kovács Árpád (1986-) (kardiológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Veress Roland (1992-) (molekuláris biológus) Horváth Balázs (1981-) (élettanász) Nagy László (1988-) (orvos) Bódi Beáta (1989-) (molekuláris biológus) Fagyas Miklós (1984-) (orvos) Helgadottir, Solveig Lind Bánhegyi Viktor (1991-) (kardiológus) Juhász Béla (1978-) (kísérletes farmakológus) Bombicz Mariann (1987-) (gyógyszerész) Priksz Dániel (1989-) (farmakológus) Nánási Péter Pál ifj. (1987-) (sejtbiológus) Merkely Béla (1965-) (orvos) Édes István (1952-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Radovits Tamás Tóth Attila (1971-) (biológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM036888
Első szerző:Hoetzenecker, Konrad
Cím:Secretome of apoptotic peripheral blood cells (APOSEC) attenuates microvascular obstruction in a porcine closed chest reperfused acute myocardial infarction model : role of platelet aggregation and vasodilation / K. Hoetzenecker, A. Assinger, M. Lichtenauer, M. Mildner, T. Schweiger, P. Starlinger, A. Jakab, E. Berényi, N. Pavo, M. Zimmermann, C. Gabriel, C. Plass, M. Gyöngyösi, I. Volf, H. J. Ankersmit
Dátum:2012
ISSN:0300-8428
Megjegyzések:Although epicardial blood flow can be restored by an early intervention in most cases, a lack of adequate reperfusion at the microvascular level is often a limiting prognostic factor of acute myocardial infarction (AMI). Our group has recently found that paracrine factors secreted from apoptotic peripheral blood mononuclear cells (APOSEC) attenuate the extent of myocardial injury. The aim of this study was to determine the influence of APOSEC on microvascular obstruction (MVO) in a porcine AMI model. A single dose of APOSEC was intravenously injected in a closed chest reperfused infarction model. MVO was determined by magnetic resonance imaging and cardiac catheterization. Role of platelet function and vasodilation were monitored by means of ELISA, flow cytometry, aggregometry, western blot and myographic experiments in vitro and in vivo. Treatment of AMI with APOSEC resulted in a significant reduction of MVO. Platelet activation markers were reduced in plasma samples obtained during AMI, suggesting an anti-aggregatory capacity of APOSEC. This finding was confirmed by in vitro tests showing that activation and aggregation of both porcine and human platelets were significantly impaired by co-incubation with APOSEC, paralleled by vasodilator-stimulated phosphoprotein (VASP)-mediated inhibition of platelets. In addition, APOSEC evidenced a significant vasodilatory capacity on coronary arteries via p-eNOS and iNOS activation. Our data give first evidence that APOSEC reduces the extent of MVO during AMI, and suggest that modulation of platelet activation and vasodilation in the initial phase after myocardial infarction contributes to the improved long-term outcome in APOSEC treated animals.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
apoptotic peripheral blood cell
myocardial infarction
Megjelenés:Basic Research in Cardiology. - 107 : 5 (2012), p. 292-305. -
További szerzők:Assinger, Alice Lichtenauer, Michael Mildner, Michael Schweiger, T. Starlinger, P. Jakab András (1985-) Berényi Ervin (1964-) (radiológus) Pavo, Noemi Zimmermann, Matthias Gabriel Ciobanu Plass, Christoph Gyöngyösi Mariann Volf, I. Ankersmit, Hendrik Jan
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM009061
Első szerző:Jost Norbert
Cím:Contribution of I Kr and I K1 to ventricular repolarization in canine and human myocytes : is there any influence of action potential duration? / Jost, N., Acsai, K., Horvath, B., Banyasz, T., Baczko, I., Bitay, M., Bogats, G., Nanasi, P. P.
Dátum:2009
ISSN:0300-8428 (Print)
Megjegyzések:The aim of the present work was to study the profile of the rapid delayed rectifier potassium current (I (Kr)) and the inward rectifier potassium current (I (K1)) during ventricular repolarization as a function of action potential duration and rate of repolarization. METHODS: Whole cell configuration of the patch clamp technique was used to monitor I (Kr) and I (K1) during the action potential plateau and terminal repolarization. Action potentials recorded at various cycle lengths (0.4-5 s) and repolarizing voltage ramps having various slopes (0.5-3 V/s) were used as command signals. I (Kr) and I (K1) were identified as difference currents dissected by E-4031 and BaCl(2), respectively. RESULTS: Neither peak amplitudes nor mean values of I (Kr) and I (K1) recorded during the plateau of canine action potentials were influenced by action potential duration. The membrane potential where I (Kr) and I (K1) peaked during the terminal repolarization was also independent of action potential duration. Similar results were obtained in undiseased human ventricular myocytes, and also in canine cells when I (Kr) and I (K1) were evoked using repolarizing voltage ramps of various slopes. Action potential voltage clamp experiments revealed that the peak values of I (Kr), I (K1), and net outward current during the terminal repolarization were independent of the pacing cycle length within the range of 0.4 and 5 s. CONCLUSIONS: The results indicate that action potential configuration fails to influence the amplitude of I (Kr) and I (K1) during the ventricular action potential in dogs and humans, suggesting that rate-dependent changes in action potential duration are not likely related to rate-dependent alterations in I (Kr) or I (K1) kinetics in these species.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Action Potentials
Animals
Barium Compounds
Chlorides
Dogs
Electrophysiology
Humans
KATP Channels
Kinetics
Muscle Cells
Patch-Clamp Techniques
Potassium Channels, Inwardly Rectifying
Reference Values
Ventricular Function
Megjelenés:Basic Research in Cardiology. - 104 : 1 (2009), p. 33-41. -
További szerzők:Acsai Károly Horváth Balázs (1981-) (élettanász) Bányász Tamás (1960-) (élettanász) Baczkó István Bitay Miklós Bogáts Gábor Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
elektronikus változat
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6.

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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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM029769
Első szerző:Lichtenauer, Michael
Cím:Secretome of apoptotic peripheral blood cells (APOSEC) confers cytoprotection to cardiomyocytes and inhibits tissue remodelling after acute myocardial infarction : a preclinical study / Lichtenauer Michael, Mildner Michael, Hoetzenecker Konrad, Zimmermann Matthias, Podesser Bruno Karl, Sipos Wolfgang, Berényi Ervin, Dworschak Martin, Tschachler Erwin, Gyöngyösi Mariann, Ankersmit Hendrik Jan
Dátum:2011
ISSN:0300-8428
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Basic Research In Cardiology. - 106 : 6 (2011), p. 1283-1297. -
További szerzők:Mildner, Michael Hoetzenecker, Konrad Zimmermann, Matthias Podesser, Bruno Karl Sipos, Wolfgang Berényi Ervin (1964-) (radiológus) Dworschak, Martin Tschachler Erwin Gyöngyösi Mariann Ankersmit, Hendrik Jan
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8.

001-es BibID:BIBFORM040606
Első szerző:Velden, Jolanda, van der
Cím:Calcium sensitivity of force in human ventricular cardiomyocytes from donor and failing hearts / van der Velden J., Boontje N. M., Papp Z., Klein L. J., Visser F. C., de Jong J. W., Owen V. J., Burton P. B., Stienen G. J.
Dátum:2002
ISSN:0300-8428
Megjegyzések:In failing human myocardium changes occur, in particular, in isoform composition and phosphorylation level of the troponin T (TnT) and troponin I (TnI) subunits of the actin filament and the myosin light chains (MLC-1 and -2), but it is unclear to what extent they influence cardiac performance. This overview concentrates on the relation between contractile function, contractile protein composition and phosphorylation levels in small biopsies from control (donor) hearts, from biopsies obtained during open heart surgery (NYHA Class I-IV) and from end-stage failing (explanted, NYHA class IV) hearts. Furthermore, attention is paid to the effect of the catalytic subunit of protein kinase A on isometric force development in single Triton-skinned human cardiomyocytes isolated from donor and end-stage failing left ventricular myocardium at different resting sarcomere lengths. A reduction in sarcomere length from 2.2 to 1.8 microm caused reductions in maximum isometric force by approximately 35% both in donor and in failing cardiomyocytes. The midpoints of the calcium sensitivity curves (pCa50) of donor and end-stage failing hearts differed markedly at all sarcomere lengths (mean delta pCa50 = 0.22). Our findings indicate that 1) TnI phosphorylation contributes to the differences in calcium sensitivity between donor and end-stage failing hearts, 2) human ventricular myocardium is heterogeneous with respect of the phosphorylation of TnT, MLC-2 and the isoform distribution of MLC-1 and MLC-2, and 3) the Frank-Starling mechanism is preserved in end-stage failing myocardium.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Basic Research In Cardiology. - 97 : Suppl.1 (2002), p. 118-126. -
További szerzők:Boontje, Nicky M. Papp Zoltán (1965-) (kardiológus, élettanász) Klein, L. J. Visser, F. C. de Jong, J. W. Owen, V. J. Burton, P. B. Stienen, Ger J. M.
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