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001-es BibID:	BIBFORM030250
035-os BibID:	WOS:000182475600002
Első szerző:	Fülöp László (kardiológus)
Cím:	Differences in electrophysiological and contractile properties of mammalian cardiac tissues bathed in bicarbonate - and HEPES-buffered solutions / L. Fülöp, G. Szigeti, J. Magyar, N. Szentandrássy, T. Ivanics, Z. Miklós, L. Ligeti, A. Kovács, G. Szénási, L. Csernoch, P. P. Nánási, T. Bányász
Dátum:	2003
ISSN:	0001-6772
Megjegyzések:	Aim: The aim of this study was to compare the action potential configuration, contractility, intracellular Ca2+ and H+ concentrations in mammalian cardiac tissues bathed with Krebs and Tyrode solutions at 37 degreesC. Results: In Langendorff-perfused guinea-pig hearts, loaded with the fluorescent Ca2+ -indicator Fura-2, or H+ -sensitive dye carboxy-SNARF, shifts from Krebs to Tyrode solution caused intra-cellular acidification, increased diastolic pressure and [Ca2+ ](i) , decreased systolic pressure and [Ca2+ ](i) , leading to a reduction in the amplitude of [Ca2+ ](i) transients and pulse pressure. Contractility was also depressed in canine ventricular trabeculae when transferred from Krebs to Tyrode solution. Shifts from Krebs to Tyrode solution increased the duration of action potentials in multicellular cardiac preparations excised from canine and rabbit hearts but not in isolated cardiomyocytes. All these changes in action potential morphology, contractility, [Ca2+ ](i) and [H+ ](i) were readily reversible by addition of 26 mmol L-1 bicarbonate to Tyrode solution. Effects of dofetilide and CsCl, both blockers of the delayed rectifier K current, on action potential duration were compared in Krebs and Tyrode solutions. Dofetilide lengthened rabbit ventricular action potentials in a significantly greater extent in Tyrode than in Krebs solution. Exposure of canine Purkinje fibres to CsCl evoked early after depolarizations within 40 min in all preparations incubated with Tyrode solution, but not in those bathed with Krebs solution. Conclusion: It is concluded that the marked differences in action potential morphology, [Ca2+ ](i) , [H+ ](i) and contractility observed between preparations bathed with Krebs and Tyrode solutions are more likely attributable to differences in the intracellular buffering capacities of the two media.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Acta Physiologica Scandinavica. - 178 : 1 (2003), p. 11-18. -
További szerzők:	Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Magyar János (1961-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Ivanics Tamás Miklós Zsuzsanna Ligeti László Kovács A. Szénási Gábor Csernoch László (1961-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Bányász Tamás (1960-) (élettanász)
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001-es BibID:	BIBFORM040624
Első szerző:	Papp Zoltán (kardiológus, élettanász)
Cím:	Calcium-dependent modulation of the plateau phase of action potential in isolated ventricular cells of rabbit heart / Papp Z., Peineau N., Szigeti G., Argibay J., Kovács L.
Dátum:	1999
ISSN:	0001-6772
Megjegyzések:	[Ca2+]i-dependent modulation of the action potential has been studied in Fura-2 dialysed ventricular myocytes of the rabbit using the whole-cell current-clamp method. Fifteen consecutive action potentials (AP1-AP15) and [Ca2+]i transients were elicited at a frequency of 0.2 Hz. A single, brief application of caffeine (during AP9) first enhanced and thereafter attenuated the [Ca2+]i transients accompanying AP9 and AP10-AP12, respectively. This approach provided direct comparison between time courses of action potentials: during the initial steady state (e.g. AP8) and when Ca2+ release from the sarcoplasmic reticulum was increased by caffeine (AP9) or decreased by depletion (AP10). The increase in [Ca2+]i facilitated repolarization and decreased action potential duration. However, action potentials at reduced Ca2+ release (AP10) had longer duration than during steady state. The caffeine-induced changes in L-type Ca2+ current (ICa,L), during voltage-clamp conditions partially explained the effects of caffeine on action potentials. When ICa,L was blocked by 500 micromol L-1 Cd2+, enhanced [Ca2+]i transients revealed an extra current component which was outward at +10 mV and inward at the resting membrane potential (most probably the transient inward current). In the presence of Cd2+, however, AP8 and AP10 had identical time courses, suggesting that ICa,L alone was responsible for the lengthening of AP10. Alterations in the transmembrane Na+ gradient resulted in changes of the steady state action potential durations (AP8) consistently with the expected modulation of the Na+-Ca2+ exchange current. However, the contribution of this current to the [Ca2+]i-dependent behaviour of action potential plateau could not be demonstrated.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Acta Physiologica Scandinavica. - 167 : 2 (1999), p. 119-129. -
További szerzők:	Peineau, N. Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Argibay, J. Kovács L.
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001-es BibID:	BIBFORM030276
035-os BibID:	WOS:000074327800003
Első szerző:	Szigligeti Péter
Cím:	Intracellular calcium and electrical restitution in mammalian cardiac cells / P. Szigligeti, T. Banyasz, J. Magyar, Gy. Szigeti, Z. Papp, A. Varro, P. P. Nanasi
Dátum:	1998
ISSN:	0001-6772
Megjegyzések:	The role of calcium current and changes in intracellular calcium concentration ([Ca(2+)](i)) in regulation of action potential duration (APD) during electrical restitution process was studied in mammalian ventricular preparations. Properly timed action potentials were recorded from multicellular preparations and isolated cardiomyocytes using conventional microelectrodes and EGTA-containing patch pipettes, APD increased monotonically in canine and guinea pig ventricular preparations with increasing diastolic interval (DI), while in rabbit papillary muscles the restitution process was biphasic: APD first lengthened, then shortened as the DI increased. When the restitution process was studied in single cardiomyocytes using EGTA-containing patch pipettes, the restitution pattern was similar in the three species studied. Similarly, no difference was observed in the recovery time constant of calcium current (/(Ca-L)) measured under these conditions in voltage clamped myocytes. Loading the myocytes with the [Ca(2+)](i)-chelator BAPTA-AM had adverse effects in rabbit and canine cells. In rabbit myocytes steady-state APD lengthened and the late shortening component of restitution was abolished in BAPTA-loaded cells. In canine myocytes BAPTA-load shortened steady-stare APD markedly, and during restitution, APD decreased with increasing DI. The late shortening component of restitution, observed in untreated rabbit preparations, was greatly reduced after nifedipine treatment, but remained preserved in the presence of 4-aminopyridine or nicorandil. Beat to beat changes in APD, peak /Ca-L and [Ca(2+)](i), measured using the fluorescent dye, Fura-2, were monitored in rabbit ventricular myocytes after a 1-min period of rest. In these cells, the shortening of APD was accompanied by a gradual reduction of the peak /Ca-L and elevation of diastolic [Ca(2+)](i) during the initial eight post-rest action potentials. it is concluded that elevation of [Ca(2+)](i) shortens, while reduction of [Ca(2+)](i) lengthens APD in rabbit, but not in canine ventricular myocytes. These differences may probably be related.io different distributions of [Ca(2+)](i)-dependent ion currents and/or to differences in calcium handling between the two species.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Acta Physiologica Scandinavica. - 163 : 2 (1998), p. 139-147. -
További szerzők:	Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Papp Zoltán (1965-) (kardiológus, élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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