| P2093 | author name string | Simurda J | |
| | Pásek M | |
| P2860 | cites work | The cardiac sodium channel: gating function and molecular pharmacology | Q28207195 |
| | The long Q-T syndrome | Q33162456 |
| | The syndrome of right bundle branch block ST segment elevation in V1 to V3 and sudden death--the Brugada syndrome | Q33935865 |
| | Cardiac sodium channel Markov model with temperature dependence and recovery from inactivation | Q34170167 |
| | Local anesthetics: hydrophilic and hydrophobic pathways for the drug-receptor reaction | Q34684384 |
| | Electrophysiological effects of diprafenone, a dimethyl congener of propafenone on guinea-pig ventricular cells | Q35871012 |
| | Na(+) channel mutation that causes both Brugada and long-QT syndrome phenotypes: a simulation study of mechanism | Q36019333 |
| | Molecular action of lidocaine on the voltage sensors of sodium channels | Q36412378 |
| | Common molecular determinants of flecainide and lidocaine block of heart Na+ channels: evidence from experiments with neutral and quaternary flecainide analogues | Q36412399 |
| | Channel openings are necessary but not sufficient for use-dependent block of cardiac Na(+) channels by flecainide: evidence from the analysis of disease-linked mutations | Q36558186 |
| | New classification of moricizine and propafenone based on electrophysiologic and electrocardiographic data from isolated rabbit heart | Q36677645 |
| | Pharmacological targeting of long QT mutant sodium channels | Q37365724 |
| | Propafenone in the treatment of cardiac arrhythmias. A risk-benefit appraisal | Q40520293 |
| | Novel arrhythmogenic mechanism revealed by a long-QT syndrome mutation in the cardiac Na(+) channel. | Q40812589 |
| | Enhanced Na(+) channel intermediate inactivation in Brugada syndrome | Q40849528 |
| | Arrhythmogenic mechanism of an LQT-3 mutation of the human heart Na(+) channel alpha-subunit: A computational analysis | Q40865508 |
| | Ionic channels in excitable membranes. Current problems and biophysical approaches | Q41862746 |
| | Block of single cardiac Na+ channels by antiarrhythmic drugs: the effect of amiodarone, propafenone and diprafenone | Q43683887 |
| | Inhibition of Na(+) current by imipramine and related compounds: different binding kinetics as an inactivation stabilizer and as an open channel blocker | Q44187768 |
| | Responsiveness of cardiac Na+ channels to antiarrhythmic drugs: the role of inactivation | Q44195022 |
| | A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction | Q45172101 |
| | Lidocaine shows greater selective depression of depolarized and acidotic myocardium than propafenone: possible implications for proarrhythmia. | Q46453123 |
| | Multiple mechanisms of Na+ channel--linked long-QT syndrome | Q49013113 |
| | Chemically modified cardiac Na+ channels and their sensitivity to antiarrhythmics: is there a hidden drug receptor? | Q51635920 |
| | Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia | Q59087954 |
| | Stereoselective interactions of (R)- and (S)-propafenone with the cardiac sodium channel | Q67541918 |
| | Use-dependent features of 4-aminopyridine block of transient outward current in rat ventricular myocytes | Q71627418 |
| | Unmasking effect of propafenone on the concealed form of the Brugada phenomenon | Q73631782 |
| | Two distinct congenital arrhythmias evoked by a multidysfunctional Na(+) channel | Q73783799 |
| P433 | issue | 2 | |
| P304 | page(s) | 151-157 | |
| P577 | publication date | 2004-03-01 | |
| P1433 | published in | Medical & Biological Engineering & Computing | Q6806252 |
| P1476 | title | Quantitative modelling of interaction of propafenone with sodium channels in cardiac cells | |
| P478 | volume | 42 | |