Action potential experiments complete hERG assay and QT-interval measurements in cardiac preclinical studies.
暂无分享,去创建一个
J. Gardette | Richard Printemps | Joffrey Ducroq | Richard Printemps | Marie Le Grand | Stephanie Guilbot | Jean Gardette | Céline Salvetat | C. Salvetat | J. Ducroq | M. Le Grand | S. Guilbot | Joffrey Ducroq | Stéphanie Guilbot
[1] H A Fozzard,et al. The relation of Vmax to INa, GNa, and h infinity in a model of the cardiac Purkinje fiber. , 1979, Biophysical journal.
[2] P. Hoffmann,et al. Are hERG channel inhibition and QT interval prolongation all there is in drug-induced torsadogenesis? A review of emerging trends. , 2006, Journal of pharmacological and toxicological methods.
[3] Hua-rong Lu,et al. Drug-induced long QT in isolated rabbit Purkinje fibers: importance of action potential duration, triangulation and early afterdepolarizations. , 2002, European journal of pharmacology.
[4] W. Crumb,et al. Drugs that prolong QT interval as an unwanted effect: assessing their likelihood of inducing hazardous cardiac dysrhythmias , 2000, Expert opinion on pharmacotherapy.
[5] C. Starmer,et al. Block of wild-type and inactivation-deficient cardiac sodium channels IFM/QQQ stably expressed in mammalian cells. , 2000, Biophysical journal.
[6] M. Sanguinetti,et al. hERG potassium channels and cardiac arrhythmia , 2006, Nature.
[7] L. Horowitz,et al. Flecainide: its proarrhythmic effect and expected changes on the surface electrocardiogram. , 1984, The American journal of cardiology.
[8] M. Omata,et al. Regional differences in transient outward current density and inhomogeneities of repolarization in rabbit right atrium. , 1995, Circulation.
[9] Jian-An Yao,et al. Dimethyl sulfoxide effects on hERG channels expressed in HEK293 cells. , 2006, Journal of pharmacological and toxicological methods.
[10] B. Sakmann,et al. Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches , 1981, Pflügers Archiv.
[11] A. Camm,et al. Relationships between preclinical cardiac electrophysiology, clinical QT interval prolongation and torsade de pointes for a broad range of drugs: evidence for a provisional safety margin in drug development. , 2003, Cardiovascular research.
[12] J. Shryock,et al. Use of preclinical assays to predict risk of drug-induced torsades de pointes. , 2005, Heart rhythm.
[13] D. Fedida,et al. The Role of Late INa and Antiarrhythmic Drugs in EAD Formation and Termination in Purkinje Fibers , 2006, Journal of cardiovascular electrophysiology.
[14] L. D. Davis,et al. Effects of flecainide on the electrophysiologic properties of isolated canine and rabbit myocardial fibers. , 1985, Journal of the American College of Cardiology.
[15] P. Kirchhof,et al. Postrepolarization refractoriness versus conduction slowing caused by class I antiarrhythmic drugs: antiarrhythmic and proarrhythmic effects. , 1998, Circulation.
[16] R. Shah,et al. Refining detection of drug-induced proarrhythmia: QT interval and TRIaD. , 2005, Heart rhythm.
[17] Richard Printemps,et al. Additive effects of ziprasidone and D,L-sotalol on the action potential in rabbit Purkinje fibres and on the hERG potassium current. , 2005, Journal of pharmacological and toxicological methods.
[18] M. Hoffmann,et al. Safety pharmacology assessment of drug-induced QT-prolongation in dogs with reduced repolarization reserve. , 2006, Journal of pharmacological and toxicological methods.
[19] Hua-rong Lu,et al. Species Plays an Important Role in Drug‐Induced Prolongation of Action Potential Duration and Early Afterdepolarizations in Isolated Purkinje Fibers , 2001, Journal of cardiovascular electrophysiology.
[20] J. Valentin,et al. Nonclinical proarrhythmia models: predicting Torsades de Pointes. , 2005, Journal of pharmacological and toxicological methods.
[21] Gary A Gintant,et al. The Utility of hERG and Repolarization Assays in Evaluating Delayed Cardiac Repolarization: Influence of Multi-Channel Block , 2004, Journal of cardiovascular pharmacology.
[22] Ard Teisman,et al. Choice of cardiac tissue plays an important role in the evaluation of drug-induced prolongation of the QT interval in vitro in rabbit. , 2005, Journal of pharmacological and toxicological methods.
[23] D. Potreau,et al. Endothelin-1 inhibits L-type Ca2+ current enhanced by isoprenaline in rat atrial myocytes. , 1997, Journal of cardiovascular pharmacology.
[24] P. Hoffmann,et al. Blinded Test in Isolated Female Rabbit Heart Reliably Identifies Action Potential Duration Prolongation and Proarrhythmic Drugs: Importance of Triangulation, Reverse Use Dependence, and Instability , 2003, Journal of cardiovascular pharmacology.
[25] C. Gibbs,et al. Papillary muscles split in the presence of 2,3-butanedione monoxime have normal energetic and mechanical properties. , 1995, The American journal of physiology.
[26] G. Duker,et al. Instability and Triangulation of the Action Potential Predict Serious Proarrhythmia, but Action Potential Duration Prolongation Is Antiarrhythmic , 2001, Circulation.
[27] S Nattel,et al. The Molecular and Ionic Specificity of Antiarrhythmic Drug Actions , 1999, Journal of cardiovascular electrophysiology.
[28] Comparative Effects of Clarithromycin on Action Potential and Ionic Currents from Rabbit Isolated Atrial and Ventricular Myocytes , 2003, Journal of cardiovascular pharmacology.
[29] A H Glassman,et al. Antipsychotic drugs: prolonged QTc interval, torsade de pointes, and sudden death. , 2001, The American journal of psychiatry.
[30] J. Hancox,et al. Inhibition of the current of heterologously expressed HERG potassium channels by flecainide and comparison with quinidine, propafenone and lignocaine , 2002, British journal of pharmacology.
[31] C. January,et al. Mechanism of block and identification of the verapamil binding domain to HERG potassium channels. , 1999, Circulation research.
[32] Charles Antzelevitch,et al. Role of transmural dispersion of repolarization in the genesis of drug-induced torsades de pointes. , 2005, Heart rhythm.
[33] R. Lazzara. From first class to third class: recent upheaval in antiarrhythmic therapy--lessons from clinical trials. , 1996, The American journal of cardiology.
[34] D. Saint,et al. BLOCK OF Na+ AND K+ CURRENTS IN RAT VENTRICULAR MYOCYTES BY QUINACAINOL AND QUINIDINE , 2005, Clinical and experimental pharmacology & physiology.
[35] Charles Antzelevitch,et al. Assessing predictors of drug-induced torsade de pointes. , 2003, Trends in pharmacological sciences.
[36] J. Tamargo. Drug-induced torsade de pointes: from molecular biology to bedside. , 2000, Japanese journal of pharmacology.