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Electrical restitution in rat ventricular muscle.
- P. Nanasi, C. Pankucsi, T. Bányász, P. Szigligeti, J. Papp, A. Varró
- Chemistry, MedicineActa physiologica Scandinavica
- 1 October 1996
It is concluded that electrical restitution in rat ventricular muscle is relatively little affected by recovery from voltage-dependent inactivation of ion channels, it is rather governed by transient changes in cytosolic Ca concentration possible via Ca-dependent Inactivation of the L-type Ca current and activation of the Na/Ca exchange current.
Differential effects of fluoxetine enantiomers in mammalian neural and cardiac tissues.
- J. Magyar, Z. Rusznák, +8 authors V. Kecskeméti
- Chemistry, MedicineInternational journal of molecular medicine
- 1 April 2003
At micromolar concentrations (between 1 and 10 microM) R(-)-fluoxetine is more effective than the S(+) enantiomer on neuronal, while less effective on cardiac calcium channels, and the stronger anticonvulsant effect of the R(-) enantiomers may be explained by these differences.
Action potential duration and force-frequency relationship in isolated rabbit, guinea pig and rat cardiac muscle
- P. Szigligeti, C. Pankucsi, T. Bányász, A. Varró, P. Nanasi
- Biology, MedicineJournal of Comparative Physiology B
It is concluded that both action potential duration and cytosolic sodium concentration are major determinants of the force-frequency relationship in mammalian myocardium.
Electrophysiological effects of fluoxetine in mammalian cardiac tissues
- P. Pacher, J. Magyar, +6 authors P. Nanasi
- Biology, MedicineNaunyn-Schmiedeberg's Archives of Pharmacology
The results suggest that fluoxetine may have antiarrhythmic (class I + IV type), as well as proarrhythmmic properties (due to impairment of atrioventricular or intraventricular conduction and shortening of repolarization) in depressed patients with cardiac disorders, and ECG control may be suggested during fluxetine therapy.
Comparative study of cardiac electrophysiological effects of atrial natriuretic peptide
- V. Kecskeméti, P. Pacher, C. Pankucsi, P. Nanasi
- Chemistry, MedicineMolecular and Cellular Biochemistry
- 1 July 1996
The present data suggest that ANP may inhibit the slow inward Ca2+ channel activity and facilitate the K+ channel Activity in atrial and guinea-pig ventricular fibers.
Electrical restitution in diseased human ventricular myocardium.
The observed changes in the restitution kinetics of the dilated human heart are, likely, the consequence of alterations in the ionic currents that underlie the cardiac action potential.
Electrophysiological effects of EGIS-7229, a new antiarrhythmic agent, in isolated mammalian and human cardiac tissues
- C. Pankucsi, T. Bányász, +5 authors P. Nanasi
- Chemistry, MedicineNaunyn-Schmiedeberg's Archives of Pharmacology
- 24 February 1997
EGIS-7229 appears to carry mixed class III, IV and IB antiarrhythmic properties in human, canine, rabbit and guinea pig cardiac preparations, but at higher concentrations also inhibits Ca and Na currents.
Electrophysiological effects of EGIS-7229, a new antiarrhythmic agent, in isolated guinea pig papillary muscle.
On the basis of present results, EGIS-7229 appears to carry mixed class I and class III characteristics; Class III properties are present at low concentrations, whereas, at higher concentrations, class I actions may be predominant.
Age-dependence of free radical-induced oxidative damage in ischemic-reperfused rat heart.
The purpose of this study was to determine the aging-induced oxidative alterations in rat heart as well as the age-dependence of heart injury following ischemia-reperfusion, andPre-treatment with a free radical scavenger, such as centrophenoxine, diminished the ischemian injury in both young and old rat hearts.
Three distinct components of the negative inotropic action of lidocaine in dog Purkinje fiber.
The negative inotropic action of lidocaine can be regarded as a sum of three distinct components: negative inotropy associated to the shortening of action potential duration per se, reduction of contractility likely due to direct inhibition of the fast sodium current and of the "window" sodium current by lidocane.