CCL

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1.

001-es BibID:BIBFORM083102
Első szerző:Kecskeméti Valéria
Cím:Can the electrophysiological action of rosiglitazone explain its cardiac side effects? / Valéria Kecskeméti, Andrea Szebeni, Norbert Szentandrássy, Péter P. Nánási
Dátum:2011
ISSN:1471-2210
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:BMC Pharmacology. - 11 : S2 (2011), p. A54. -
További szerzők:Szebeni Andrea Szentandrássy Norbert (1976-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
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2.

001-es BibID:BIBFORM030340
035-os BibID:WOS:A1996VM24200008 PMID:8901455
Első szerző:Kecskeméti Valéria
Cím:Comparative study of cardiac electrophysiological effects of atrial natriuretic peptide / Valéria Kecskemeti, Pál Pacher, Csaba Pankucsi, Péter P. Nanasi
Dátum:1996
ISSN:0300-8177
Megjegyzések:The effects of atrial natriuretic peptide (ANP) on action potential characteristics were studied in various (human, rabbit, guineapig) atrial and guinea-pig right ventricular papillary muscles. ANP (1-100 nM) did not modify the resting membrane potential nor the maximum rate of depolarization phase (V-max). Up to 10 nM, ANP dose-dependently decreased the action potential amplitude both in guinea-pig atrial and ventricular muscles, but it did not affect this parameter in the other atrial preparations. ANP caused a dose-dependent, marked decrease of action potential duration (APD) in practically every cardiac preparation studied (exception of guinea-pig left atrium). The strongest effect on APD can be observed in human atrial and guinea-pig ventricular fibers. The K+ channel blocker 4-aminopyridine (1 mM) and the ATP-dependent K+ channel inhibitor glibenclamide (10 mu M) prevented the effect of ANP on APD in both ventricular atrial preparations. ANP prevented the appearance of isoprenaline (0.5 mu M) induced slow AP in K+ depolarized myocardium. The present data suggest that ANP may inhibit the slow inward Ca2+ channel activity and facilitate the K+ channel activity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Molecular and Cellular Biochemistry. - 160-161 (1996), p. 53-59. -
További szerzők:Pacher Pál Pankucsi Csaba (farmakológus) Nánási Péter Pál (1956-) (élettanász)
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3.

001-es BibID:BIBFORM018458
Első szerző:Kecskeméti Valéria
Cím:Norfluoxetine and fluoxetine have similar anticonvulsant and Ca channel blocking potencies / Kecskeméti V., Rusznák Z., Riba P., Pál B., Wagner R., Harasztosi C., Nánási P. P., Szűcs G.
Dátum:2005
ISSN:0361-9230
Megjegyzések:Norfluoxetine is the most important active metabolite of the widely used antidepressant fluoxetine but little is known about its pharmacological actions. In this study the anticonvulsant actions of norfluoxetine and fluoxetine were studied and compared to those of phenytoin and clonazepam in pentylenetetrazol-induced mouse epilepsy models. Pretreatment with fluoxetine or norfluoxetine (20 mg/kg s.c.), as well as phenytoin (30 mg/kg s.c.) and clonazepam (0.1 mg/kg s.c.) significantly increased both the rate and duration of survival, demonstratinga significant protective effect against pentylenetetrazol-induced epilepsy. These effects of norfluoxetine were similar to those of fluoxetine. According to the calculated combined protection scores, both norfluoxetine and fluoxetine were effective from the concentration of 10 mg/kg,while the highest protective action was observed with clonazepam. Effects of norfluoxetine and fluoxetine on voltage-gated Ca2+ channels were evaluated by measuring peak Ba2+ current flowing through the Ca2+ channels upon depolarization using whole cell voltage clamp in enzymatically isolated rat cochlear neurons. The current was reduced equally in a concentration-dependent manner by norfluoxetine (EC50 = 20.4?2.7M, Hill coefficient = 0.86?0.1) and fluoxetine(EC50 = 22.3?3.6M, Hill coefficient = 0.87?0.1). It was concluded that the efficacy of the two compounds in neuronal tissues was equal, either in preventing seizure activity or in blockingthe neuronal Ca2+ channels.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Fluoxetine
Norfluoxetine
Anticonvulsants
Neuronal Ca2+ currents
Voltage clamp
Megjelenés:Brain Research Bulletin. - 67 : 1-2 (2005), p. 126-132. -
További szerzők:Rusznák Zoltán (1965-) (élettanász) Riba Pál Pál Balázs (1975-) (élettanász) Wagner Róbert Harasztosi Csaba Nánási Péter Pál (1956-) (élettanász) Szűcs Géza (1948-) (élettanász)
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4.

001-es BibID:BIBFORM049179
035-os BibID:PMID:23588116 WOS:000319508800002
Első szerző:Kistamás Kornél (biológus)
Cím:Effects of pioglitazone on cardiac ion currents and action potential morphology in canine ventricular myocytes / Kornél Kistamás, Norbert Szentandrássy, Bence Hegyi, Ferenc Ruzsnavszky, Krisztina Váczi, László Bárándi, Balázs Horváth, Andrea Szebeni, János Magyar, Tamás Bányász, Valéria Kecskeméti, Péter P. Nánási
Dátum:2013
ISSN:0014-2999
Megjegyzések:Despite its widespread therapeutical use there is little information on the cellular cardiac effects of the antidiabetic drug pioglitazone in larger mammals. In the present study, therefore, the concentration-dependent effects of pioglitazone on ion currents and action potential configuration were studied in isolated canine ventricular myocytes using standard microelectrode, conventional whole cell patch clamp, and action potential voltage clamp techniques. Pioglitazone decreased the maximum velocity of depolarization and the amplitude of phase-1 repolarization at concentrations ?3 ?M. Action potentials were shortened by pioglitazone at concentrations ?10 ?M, which effect was accompanied with significant reduction of beat-to-beat variability of action potential duration. Several transmembrane ion currents, including the transient outward K+ current (Ito), the L-type Ca2+ current (ICa), the rapid and slow components of the delayed rectifier K+ current (IKr and IKs, respectively), and the inward rectifier K+ current (IK1) were inhibited by pioglitazone under conventional voltage clamp conditions. Ito was blocked significantly at concentrations ?3 ?M, ICa, IKr, IKs at concentrations ?10 ?M, while IK1 at concentrations ?30 ?M. Suppression of Ito, ICa, IKr, and IK1 has been confirmed also under action potential voltage clamp conditions. ATP-sensitive K+ current, when activated by lemakalim, was effectively blocked by pioglitazone. Accordingly, action potentials were prolonged by 10 ?M pioglitazone when the drug was applied in the presence of lemakalim. All these effects developed rapidly and were readily reversible upon washout. In conclusion, pioglitazone seems to be a harmless agent at usual therapeutic concentrations.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Antidiabetic agents
Pioglitazone
Dog cardiomyocytes
Action potentials
Ion currents
Megjelenés:European Journal of Pharmacology. - 710 : 1-3 (2013), p. 10-19. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Hegyi Bence (1987-) (élettanász) Ruzsnavszky Ferenc (1984-) (élettanász) Váczi Krisztina (1987-) (élettanász) Bárándi László (1984-) (élettanász) Horváth Balázs (1981-) (élettanász) Szebeni Andrea Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K100151
OTKA
NK104331
OTKA
K101196
OTKA
PD101171
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Élettan Kutatócsoport
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5.

001-es BibID:BIBFORM009079
Első szerző:Lengyel Csaba (Szeged)
Cím:Role of slow delayed rectifier K+-current in QT prolongation in the alloxan-induced diabetic rabbit heart / Lengyel, C., Virag, L., Kovacs, P. P., Kristof, A., Pacher, P., Kocsis, E., Koltay, Z. M., Nanasi, P. P., Toth, M., Kecskemeti, V., Papp, J. G., Varro, A., Jost, N.
Dátum:2008
ISSN:1748-1716 (Electronic)
Megjegyzések:In diabetes mellitus, several cardiac electrophysiological parameters are known to be affected. In rodent experimental diabetes models, changes in these parameters were reported, but only limited relevant information is available in other species, having cardiac electrophysiological properties more resembling the human, including the rabbit. The present study was designed to analyse the effects of experimental type 1 diabetes on ventricular repolarization and the underlying transmembrane potassium currents in rabbit hearts. METHODS: Diabetes was induced by a single injection of alloxan (145 mg kg(-1) i.v.). After the development of diabetes (3 weeks), electrophysiological studies were performed using whole cell voltage clamp and ECG measurements. RESULTS: The QT(c) interval in diabetic rabbits was moderately but statistically significantly longer than measured in the control animals (155 +/- 1.8 ms vs. 145 +/- 2.8 ms, respectively, n = 9-10, P < 0.05). This QT(c)-lengthening effect of diabetes was accompanied by a significant reduction in the density of the slow delayed rectifier K(+) current, I(Ks) (from 1.48 +/- 0.35 to 0.86 +/- 0.17 pA pF(-1) at +50 mV, n = 19-21, P < 0.05) without changes in current kinetics. No differences were observed either in the density or in the kinetics of the inward rectifier K(+) current (I(K1)), the rapid delayed rectifier K(+) current (I(Kr)), the transient outward current (I(to)) and the L-type calcium current (I(CaL)) between the control and alloxan-treated rabbits. CONCLUSION: It is concluded that type 1 diabetes mellitus, although only moderately, lengthens ventricular repolarization. Diabetes attenuates the repolarization reserve by decreasing the density of I(Ks) current, and thereby may enhance the risk of sudden cardiac death.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Alloxan
Animals
Delayed Rectifier Potassium Channels
Diabetes Mellitus, Experimental
Electrocardiography
Heart
Heart Conduction System
Heart Ventricles
Long QT Syndrome
Male
Patch-Clamp Techniques
Rabbits
Megjelenés:Acta Physiologica (Oxford, England). - 192 : 3 (2008), p. 359-368. -
További szerzők:Virág László (élettanász Szeged) Kovacs Péter Pál (Szeged) Kristóf A. (Szeged) Pacher Pál Kocsis E. Koltay Zs. M. Nánási Péter Pál (1956-) (élettanász) Tóth M. Kecskeméti Valéria Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Jost Norbert
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elektronikus változat
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6.

001-es BibID:BIBFORM001024
Első szerző:Lengyel Csaba (Szeged)
Cím:Diabetes mellitus attenuates the repolarization reserve in mammalian heart / Lengyel Cs., Virág L., Bíró T., Jost N., Magyar J., Biliczki P., Kocsis E., Skoumal R., Nánási P.P., Tóth M., Kecskeméti V., Papp Gy. J., Varró A.
Dátum:2007
ISSN:0008-6363 (Print)
Megjegyzések:In diabetes mellitus several cardiac electrophysiological parameters are known to be affected. In rodent experimental diabetes models changes in these parameters were reported, but no such data are available in other mammalian species including the dog. The present study was designed to analyse the effects of experimental type 1 diabetes on ventricular repolarization and its underlying transmembrane ionic currents and channel proteins in canine hearts. METHODS AND RESULTS: Diabetes was induced by a single injection of alloxan, a subgroup of dogs received insulin substitution. After the development of diabetes (8 weeks) electrophysiological studies were performed using conventional microelectrodes, whole cell voltage clamp, and ECG. Expression of ion channel proteins was evaluated by Western blotting. The QTc interval and the ventricular action potential duration in diabetic dogs were moderately prolonged. This was accompanied by significant reduction in the density of the transient outward K+ current (I(to)) and the slow delayed rectifier K+ current (I(Ks)), to 54.6% and 69.3% of control, respectively. No differences were observed in the density of the inward rectifier K+ current (I(K1)), rapid delayed rectifier K+ current (I(Kr)), and L-type Ca2+ current (I(Ca)). Western blot analysis revealed a reduced expression of Kv4.3 and MinK (to 25+/-21% and 48+/-15% of control, respectively) in diabetic dogs, while other channel proteins were unchanged (HERG, MiRP1, alpha(1c)) or increased (Kv1.4, KChIP2, KvLQT1). Insulin substitution fully prevented the diabetes-induced changes in I(Ks), KvLQT1 and MinK, however, the changes in I(to), Kv4.3, and Kv1.4 were only partially diminished by insulin. CONCLUSION: It is concluded that type 1 diabetes mellitus, although only moderately, lengthens ventricular repolarization, attenuates the repolarization reserve by decreasing I(to) and I(Ks) currents, and thereby may markedly enhance the risk of sudden cardiac death.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardiovascular Research 73 : 3 (2007), p. 512-520. -
További szerzők:Virág László (élettanász Szeged) Bíró Tamás (1968-) (élettanász) Jost Norbert Magyar János (1961-) (élettanász) Biliczki Péter Kocsis E. Skoumal, R. Nánási Péter Pál (1956-) (élettanász) Tóth M. Kecskeméti Valéria Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus)
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7.

001-es BibID:BIBFORM030258
035-os BibID:WOS:000181565400020
Első szerző:Magyar János (élettanász)
Cím:Differential effects of fluoxetine enantiomers in mammalian neural and cardiac tissues / János Magyar, Zoltán Rusznák, Csaba Harasztosi, Ágnes Körtvély, Pál Pacher, Tamás Bányász, Csaba Pankucsi, László Kovács, Géza Szűcs, Péter P. Nánási, Valéria Kecskeméti
Dátum:2003
ISSN:1107-3756
Megjegyzések:Racemic fluoxetine is a widely used SSRI antidepressant compound having also anticonvulsant effect. In addition, it was shown that it blocked several types of voltage gated ion channels including neural and cardiac calcium channels. In the present study the effects of enantiomers of fluoxetine (R(-)-fluoxetine and S(+)-fluoxetine) were compared on neuronal and cardiac voltage-gated Ca2+ channels using the whole cell configuration of patch clamp techniques, and the anticonvulsant action of these enantiomers was also evaluated in a mouse epilepsy model. In isolated pyramidal neurons of the dorsal cochlear nucleus of the rat the effect of fluoxetine (S(+), R(-) and racemic) was studied on the Ca2+ channels by measuring peak Ba2+ current during ramp depolarizations. All forms of fluoxetine reduced the Ba2+ current of the pyramidal cells in a concentration-dependent manner, with a K, value of 22.3 +/- 3.6 muM for racemic fluoxetine. This value of K, was higher by one order of magnitude than found in cardiac myocytes with fluoxetine enantiomers (2.4 +/- 0.1 and 2.8 +/- 0.2 muM). Difference between the effects of the two enantiomers on neuronal Ba2+, current was observed only at 5 muM concentration: R(-)-fluoxetine inhibited 28 +/- 3% of the peak current, while S(+)-fluoxetine reduced the current by 18 +/- 2% (n=13, P<0.05). In voltage clamped canine ventricular cardiomyocytes both enantiomers of fluoxetine caused a reversible concentration-dependent block of the peak Ca2+ current measured at 0 mV. Significant differences between the two enantiomers in this blocking effect was observed at low concentrations only: S(+)-fluoxetine caused a higher degree of block than R(-)-fluoxetine (56.3 +/- 2.2% versus 49.1 +/- 2.2% and 95.5 +/- 0.9% versus 84.5 +/- 3.1% block with 3 and 10 &mu;M S(+) and R(-)-fluoxetine, respectively, P<0.05, n=5). Studied in current clamp mode, micromolar concentrations of fluoxetine shortened action potential duration of isolated ventricular cells, while higher concentrations also suppressed maximum velocity of depolarization and action potential amplitude. This shortening effect was significantly greater in the case of S(+) than R(-)-fluoxetine at 1 and 3 muM concentrations, whereas no differences in their effects on depolarization were observed. In pentylenetetrazole-induced mouse epilepsy model fluoxetine pretreatment significantly increased the 60 min survival rate, survival duration and seizure latency. These effects were more pronounced with the R(-) than the S(+) enantiomer. The results indicate that fluoxetine exerts much stronger suppressive effect on cardiac than neuronal calcium channels. At micromolar concentrations (between 1 and 10 muM) R(-)-fluoxetine is more effective than the S(+) enantiomer on neuronal, while less effective on cardiac calcium channels. The stronger anticonvulsant effect of the R(-) enantiomer may, at least partially, be explained by these differences. Used as an antidepressant or anticonvulsant drug, less severe cardiac side-effects are anticipated with the R(-) enantiomer.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:International Journal of Molecular Medicine. - 11 : 4 (2003), p. 535-542. -
További szerzők:Rusznák Zoltán (1965-) (élettanász) Harasztosi Csaba Körtvély Ágnes Pacher Pál Bányász Tamás (1960-) (élettanász) Pankucsi Csaba (farmakológus) Kovács László (1939-) (élettanász) Szűcs Géza (1948-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Kecskeméti Valéria
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8.

001-es BibID:BIBFORM030256
035-os BibID:WOS:000178499200009
Első szerző:Magyar János (élettanász)
Cím:Electrophysiological effects of risperidone in mammalian cardiac cells / János Magyar, Tamás Bányász, Zsolt Bagi, Pál Pacher, Norbert Szentandrássy, László Fülöp, Valéria Kecskeméti, Péter P. Nánási
Dátum:2002
ISSN:0028-1298
Megjegyzések:In this study, the effects of risperidone, the widely used antipsychotic drug, on isolated canine ventricular myocytes and guinea-pig papillary muscles were analyzed using conventional microelectrode and whole cell voltage-clamp techniques. Risperidone concentration-dependently lengthened action potential duration in guinea-pig papillary muscles (EC50=0.29 +/- 0.02 muM) and single canine ventricular myocytes (EC50=0.48 +/- 0.14 muM). This effect was reversible, showed reverse rate dependence, and it was most prominent on the terminal portion of repolarization. No significant effect of risperidone on the resting membrane potential, action potential amplitude or maximum rate of depolarization was observed. In voltage-clamped canine ventricular myocytes risperidone caused concentration-dependent block of the rapid component of the delayed rectifier K+ current (1(Kr)), measured as outward current tails at -40 mV with an IC50 of 0.92 +/- 0.26 muM. Suppression of I-Kr was not associated with changes in activation or deactivation kinetics. High concentration of risperidone (10 muM) suppressed also the slow component of the delayed rectifier K+ current (I-Ks) by 9.6 +/- 1.5% at +50 mV. These effects of risperidone developed rapidly and were readily reversible. Risperidone had no significant effect on the amplitude of other K+ currents (I-K1 and I-to). The inhibition of cardiac I-Kr current by risperidone may explain the cardiac side-effects observed occasionally with the drug. Our results suggest that risperidone displays class III antiarrhythmic properties, and as such, may produce QTc prolongation, especially in patients with long QT syndrome. Therefore, in psychotic patients having also cardiac disorders, ECG control may be suggested during risperidone therapy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 366 : 4 (2002), p. 350-356. -
További szerzők:Bányász Tamás (1960-) (élettanász) Bagi Zsolt (1974-) (orvos) Pacher Pál Szentandrássy Norbert (1976-) (élettanász) Fülöp László (1976-) (kardiológus) Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
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Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM030244
035-os BibID:WOS:000224528800006
Első szerző:Magyar János (élettanász)
Cím:Effects of norfluoxetine on the action potential and transmembrane ion currents in canine ventricular cardiomyocytes / János Magyar, Norbert Szentandrassy, Tamás Banyasz, Valéria Kecskemeti, Péter P. Nanasi
Dátum:2004
ISSN:0028-1298
Megjegyzések:Norfluoxetine is the most important active metabolite of the widely used antidepressant compound fluoxetine. Although the cellular electrophysiological actions of fluoxetine are well characterized in cardiac cells, little is known about the effects of its metabolite. In this study, therefore, the effects of norfluoxetine on action potential (AP) configuration and transmembrane ion currents were studied in isolated canine cardiomyocytes using the whole cell configuration of patch clamp techniques. Micromolar concentrations of norfluoxetine (1-10 muM) modified AP configuration: amplitude and duration of the AP and maximum velocity of depolarization were decreased in addition to depression of the plateau and elimination of the incisura of AP. Voltage clamp experiments revealed a concentration-dependent suppression of both L-type Ca2+ current, I-Ca (EC50=1.13 +/-10.08 muM) and transient outward K+ current, I-to (EC50=1.19+/-0.17 muM) having Hill coefficients close to unity. The midpoint potential of the steady-state inactivation of I-Ca was shifted from -20.9+/-0.75 mV to -27.7 +/-1.35 mV by 3 muM norfluoxetine (P<0.05, n=7). No such shift in the steady-state inactivation curve was observed in the case of I-to. Similarly, norfluoxetine caused no change in the steady-state current-voltage relationship of the membrane or in the density of the inward rectifier K+ current, I-Kl. All these effects of norfluoxetine developed rapidly and were fully reversible. Comparing present results with those obtained previously with fluoxetine, it can be concluded that norfluoxetine displays stronger suppression of cardiac ion channels than fluoxetine. Consequently, the majority of the cardiac side effects observed during fluoxetine treatment are likely to be attributed to its metabolite norfluoxetine.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 370 : 3 (2004), p. 203-210. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász) Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

10.

001-es BibID:BIBFORM030213
035-os BibID:WOS:000294414700001
Első szerző:Nánási Péter Pál (élettanász)
Cím:Hot topic : hot topics in cellular cardiac electrophysiology with potential impact on future drug design / Péter P. Nánási, Valéria Kecskeméti
Dátum:2011
ISSN:0929-8673
Tárgyszavak:Orvostudományok Elméleti orvostudományok szerkesztőségi anyag
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3595-3596. -
További szerzők:Kecskeméti Valéria
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

11.

001-es BibID:BIBFORM030332
035-os BibID:WOS:000080469500003
Első szerző:Pacher Pál
Cím:Speculations on difference between tricyclic and selective serotonin reuptake inhibitor antidepressants on their cardiac effects : Is there any? / Pal Pacher, Zoltan Ungvari, Peter P. Nanasi, Susanna Furst, Valeria Kecskemeti
Dátum:1999
ISSN:0929-8673
Megjegyzések:The cardiovascular effects and toxicity of tricyclic antidepressants (TCAs) have been well documented in medical literature. The most common manifestation of such effects is slowing of intraventricular conduction, manifested by prolonged PR, QRS and QT intervals on the standard electrocardiogram (ECG) and postural hypotension. In contrast to TCAs; selective serotonin reuptake inhibitors (SSRIs), including fluoxetine and citalopram, are considered to cause less effect on cardiac impulse conduction. In addition, these compounds induced significantly less anticholinergic, antihistaminergic and cardiotoxic side-effects than TCAs. However, there is an increasing number of case reports on dysrhythmias, like atrial fibrillation or bradycardia and syncope associated with fluoxetine and another SSRI treatment and overdose. Although such reports have not been common, they do raise concerns. In cardiac tissues isolated from canine, rabbit, rat and guinea pig hearts we have found that fluoxetine and citalopram inhibited cardiac Na+ and Ca2+ channels. These direct cardiac electrophysiological effects were similar to those of observed for tricyclic antidepressants clomipramine and imipramine. The inhibition of cardiac Ca2+ and Na+ channels by fluoxetine may explain most cardiac side-effects observed occasionally with the drug and mild but significant bradycardia reported during chronic treatment. Our results suggest that fluoxetine and citalopram may have antiarrhythmic (class I + IV type), as well as proarrhythmic properties (due to impairment of atrioventricular or intraventricular conduction and shortening of repolarization). Taking all these into consideration, in depressed patients having also severe cardiac disorders, ECG control may be suggested during fluoxetine and probable another SSRI therapy. The primary goal of this review is to compare these direct cardiac effects of fluoxetine and citalopram to those of previously reported for TCAs. This paper also summarizes the recently observed effects of fluoxetine apparently not related to the blockage of 5-HT transporter based on literature.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current Medicinal Chemistry. - 6 : 6 (1999), p. 469-480. -
További szerzők:Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Furst, Susanna Kecskeméti Valéria
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM030273
Első szerző:Pacher Pál
Cím:Electrophysiological changes in rat ventricular and atrial myocardium at different stages of experimental diabetes / P. Pacher, Z. Ungvari, P. P. Nanasi, V. Kecskemeti
Dátum:1999
ISSN:0001-6772
Megjegyzések:Action potential configuration in ventricular and atrial myocardium, as well as rate-dependent changes in ventricular action potential duration (APD) were studied and compared in healthy and diabetic rats. Diabetes was induced by a single injection of streptozotocin (STZ, 65 mg kg(-1) i.v.). Conventional microelectrode techniques were applied to record action potentials after the establishment of diabetes (2, 6, 10 and 18 weeks after STZ-treatment). Untreated age-matched animals were used as controls. Both depolarization and repolarization were significantly retarded following STZ-treatment. However, the time course of development of diabetic changes in atrial and ventricular myocardium was different. APD was significantly lengthened from week 2 of diabetes in ventricular; but only from week 6 in atrial preparations. In atrial myocardium. lengthening of APD was more pronounced at early rather than late phases of repolarization.,The maximum rate of depolarization (V-max) was significantly reduced from the 6th week of diabetes in both preparations. No differences were observed in action potential amplitude (except at week 18) and in the resting membrane potential in diabetic rats. Diabetic ventricular preparations showed a positive APD-frequency relationship at any level of repolarization. in contrast to control muscles, where APD(25) and APD(50) values lengthened. But APD(75) and APD(90) values were not changed significantly with increase in the pacing frequency. The results indicate that development of diabetic alterations are not fully identical in atrial and ventricular myocardium of the rat, probably owing to differences in density and kinetics of ionic currents responsible for atrial and ventricular action potentials.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Acta Physiologica Scandinavica. - 166 : 1 (1999), p. 7-13. -
További szerzők:Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Kecskeméti Valéria
Internet cím:elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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