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1.

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
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2.

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
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3.

001-es BibID:BIBFORM030272
Első szerző:Pacher Pál
Cím:Post-partum prolongation of the atrial repolarization in rabbit / P. Pacher, Z. Ungvari, P. P. Nanasi, I. Mucha, V. Kecskemeti, Gy. Losonczy
Dátum:1999
ISSN:0001-6772
Megjegyzések:Female sexual steroids are known to modify the expression of various K+ channels and thus they can alter cardiac repolarization. In the present work, using conventional microelectrode techniques, action potential characteristics were studied in atrial myocardium isolated from virgin, late pregnant, early (1-3 days) post-partum and late (2-3 weeks) post-partum rabbits. No changes in action potential configuration were observed during pregnancy. However, the duration, overshoot and amplitude of action potentials were significantly increased in the early (1-3 days) post-partum period. Resting potential and maximum rate of depolarization remained unchanged. The observed changes were transient, normal action potential characteristics were obtained at weeks 2-3 post-partum. 4-aminopyridine (1 mmol L-1). caused a marked lengthening of action potential duration in all preparations obtained from non-pregnant and pregnant rabbits, whereas this 4-aminopyridine-induced prolongation was moderate in those preparations excised from the hearts of early post-partum animals. Action potential configuration was not affected by pinacidil (10 mu mol L-1) or glibenclamide (5 mu mol L-1) in non-pregnant or pregnant animals. In preparations obtained from early post-partum rabbits, pinacidil significantly shortened action potential duration, which was reverted by glibenclamide. The lengthening of action potential duration together with the decreased sensitivity to 4-aminopyridine observed in early post-partum animals may probably be caused by reduction of the transient outward K+ current at this stage. The results also suggest that electrophysiological alterations in the early post-partum period may probably be more pronounced than those associated with pregnancy itself.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Acta Physiologica Scandinavica. - 166 : 1 (1999), p. 1-5. -
További szerzők:Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Mucha, I. Kecskeméti Valéria Losonczy György
Internet cím:elektronikus változat
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4.

001-es BibID:BIBFORM030271
Első szerző:Pacher Pál
Cím:Cardiac electrophysiological effects of citalopram in guinea pig papillary muscle comparison with clomipramine / Pál Pacher, Zsolt Bagi, Zoltán Lako-Futo, Zoltán Ungvari, Péter P. Nanasi, Valéria Kecskemeti
Dátum:2000
ISSN:0306-3623
Megjegyzések:The effect of citalopram, a selective serotonin reuptake inhibitor (SSRI) antidepressant, was studied on cardiac action potential configuration and compared with that of the tricyclic antidepressant (TCA) clomipramine. Conventional microelectrode techniques were used in right ventricular papillary muscle preparations of the guinea pig. Citalopram caused a concentration-dependent (10-100 mu M) shortening of action potential duration (APD), depression of plateau and overshoot potential, and reduction of maximum velocity of depolarization (V-max). No significant changes in resting membrane potential were observed. Similar results were obtained with clomipramine; however, reduction of V-max and overshoot was more pronounced with clomipramine, whereas citalopram caused relatively greater shortening of APD. Effects of both drugs were partly reversible. The results indicate that the SSRI antidepressant citalopram, similarly to TCA compounds, alters cardiac action potential configuration in guinea pig ventricular muscle, probably owing to inhibition of cardiac Na+ and Ca2+ channels. Differences in cardiac side effects of the two drugs may be related to their different actions on cardiac action potential configuration. (C) 2000 Elsevier Science inc. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Pharmacology. - 34 : 1 (2000), p. 17-23. -
További szerzők:Bagi Zsolt (1974-) (orvos) Lakó-Futó Zoltán Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Kecskeméti Valéria
Internet cím:DOI
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5.

001-es BibID:BIBFORM030266
035-os BibID:WOS:000084701100010
Első szerző:Pacher Pál
Cím:Electrophysiological effects of fluoxetine in mammalian cardiac tissues / Pál Pacher, János Magyar, Péter Szigligeti, Tamás Bányász, Csaba Pankucsi, Zsuzsanna Korom, Zoltán Ungvári, Valéria Kecskeméti, Péter P. Nánási
Dátum:2000
ISSN:0028-1298
Megjegyzések:Fluoxetine is a widely used antidepressant compound having selective serotonin reuptake inhibitor properties. In this study, the actions of fluoxetine were analyzed in guinea pig, rat, rabbit and canine ventricular myocardiac preparations using conventional microelectrode and whole cell voltage clamp techniques. Low concentrations of fluoxetine (1-10 mu mol/l) caused significant shortening of action potential duration (APD) and depression of the plateau potential in guinea pig and rabbit papillary muscles and single canine ventricular myocytes. In rat papillary muscle, APD was not affected by fluoxetine (up to 100 mu mol/l), however, the drug decreased the force of contraction with EC50 of 10 mu mol/l. Fluoxetine (10 mu mol/l) also decreased the maximum velocity of depolarization and action potential overshoot in each species studied. At this concentration no effect was observed on the resting membrane potential; high concentration (100 mu mol/l), however, caused depolarization. In voltage clamped canine ventricular myocytes, fluoxetine caused concentration-dependent block of the peak Ca2+ current at 0 mV with EC50 Of 5.4+/-0.94 mu mol/l and Hill coefficient of 1.1+/-0.14 (n=6). In addition, 10 mu mol/l fluoxetine shifted the midpoint of the steady-state inactivation curve of the Ca2+ current from -20.7+/-0.65 to -26.7+/-1 mV (P<0.001, n=8) without changing its slope factor. These effects of fluoxetine developed rapidly and were fully reversible. Fluoxetine did not alter voltage-dependence of activation or time constant for inactivation of I-Ca. Fluoxetine had no effect on the amplitude of K+ currents (I-K1 and I-to). The inhibition of cardiac Ca2+ and Na+ channels by fluoxetine may explain most cardiac side effects observed occasionally with the drug. Our results suggest that fluoxetine may have antiarrhythmic (class I + IV type), as well as proarrhythmic properties (due to impairment of atrioventricular or intraventricular conduction and shortening of repolarization). Therefore, in depressed patients with cardiac disorders, ECG control may be suggested during fluoxetine therapy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 361 : 1 (2000), p. 67-73. -
További szerzők:Magyar János (1961-) (élettanász) Szigligeti Péter Bányász Tamás (1960-) (élettanász) Pankucsi Csaba (farmakológus) Korom Zsuzsanna Ungvári Zoltán Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
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