The Experts below are selected from a list of 363 Experts worldwide ranked by ideXlab platform
Feliksas F Bukauskas - One of the best experts on this subject based on the ideXlab platform.
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connexin mediated cardiac impulse propagation connexin 30 2 slows atrioventricular conduction in mouse heart
Trends in Cardiovascular Medicine, 2006Co-Authors: Maria M Kreuzberg, Feliksas F Bukauskas, Klaus WilleckeAbstract:In mouse heart, four connexins (Cxs), Cx30.2, Cx40, Cx43, and Cx45, form gap junction (GJ) channels for electric and metabolic cell-to-cell signaling. Extent and pattern of Cx isoform expression together with cytoarchitecture and excitability of cells determine the velocity of excitation spread in different regions of the heart. In the SA node, cell–cell coupling is mediated by Cx30.2 and Cx45, which form low-conductance (approximately 9 and 32 pS, respectively) GJ channels. In contrast, the working cardiomyocytes of atria and ventricles express mainly Cx40 and Cx43, which form GJ channels of high conductance (approximately 180 and 115 pS, respectively) that facilitate the fast conduction necessary for efficient mechanical contraction. In the AV node, cell–cell coupling is mediated by abundantly expressed Cx30.2 and Cx45 and Cx40, which is expressed to a lesser extent. Cx30.2 and Cx45 may determine higher intercellular resistance and slower conduction in the SA- and AV-nodal regions than in the ventricular conduction system or the atrial and ventricular working myocardium. Cx30.2 and its putative human ortholog, Cx31.9, under physiologic conditions form unapposed hemichannels in nonjunctional plasma membrane; these hemichannels have a conductance of approximately 20 pS and are permeable to cationic dyes up to approximately 400 Da in molecular mass. Genetic ablation of Cxs confirmed that Cx40 and Cx43 are important in determining the high conduction velocities in atria and ventricles, whereas the deletion of the Cx30.2 complementary DNA led to accelerated conduction in the AV node and reduced the Wenckebach Period. We suggest that these effects are caused by (1) a dominant-negative effect of Cx30.2 on junctional conductance via formation of low-conductance homotypic and heterotypic GJ channels, and (2) open Cx30.2 hemichannels in non-junctional membranes, which shorten the space constant and depolarize the excitable membrane.
Robert J. Myerburg - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms and dynamics of episodes of progression of 2:1 atrioventricular block in patients with documented two-level conduction disturbances.
American Journal of Cardiology, 1992Co-Authors: Agustin Castellanos, Alberto Interian, Manuel Mayor, Tomas Ravina, Pedro Fernández, Robert J. MyerburgAbstract:Abstract Twenty episodes of progression of 2:1 atrioventricular (AV) block were identified during incremental atrial stimulation in 7 patients with documented (2-level) block in the AV node and His-Purkinje system. All occurred at cycle lengths shorter than those at which stable 2:1 HV block had been detected. Thirteen episodes were typical since 2:1 increased to 3:1 AV Mock when an atrio-His (AH) Wenckebach Period was completed with an atrial impulse that otherwise would have been conducted. These episodes occurred with dynamic A(M): V(N) ratios similar to those seen at the AV node. Seven atypical episodes were identified (while AH Wenckebach Periods were occurring): (1) 2:1 increasing to 3:1 AV block and then to 4:1 AV block resulting from prolonged refractoriness in the His-Purkinje system subsequently followed by concealed conduction in the latter structure; (2) conversion of 3:2 directly into 3:1 AV block due to block of the next-to-last atrial impulse in the His-Purkinje system with completion of AH Wenckebach Period with the following atrial impulse; and (3) 4:2 AV block presumably due to supernormal conduction in a transversely dissociated His-Purkinje system. These episodes occurred with A(M): V(N) ratios, which in other structures would have been indicative of different degrees of AV block. In conclusion, progression of 2:1 AV block during documented 2 level conduction disturbances (1) can be explained by mechanisms different than those currently known, and (2) has rich, but different dynamics from those observed exclusively in the AV node and exclusively in the His-Purkinje system.
Klaus Willecke - One of the best experts on this subject based on the ideXlab platform.
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connexin mediated cardiac impulse propagation connexin 30 2 slows atrioventricular conduction in mouse heart
Trends in Cardiovascular Medicine, 2006Co-Authors: Maria M Kreuzberg, Feliksas F Bukauskas, Klaus WilleckeAbstract:In mouse heart, four connexins (Cxs), Cx30.2, Cx40, Cx43, and Cx45, form gap junction (GJ) channels for electric and metabolic cell-to-cell signaling. Extent and pattern of Cx isoform expression together with cytoarchitecture and excitability of cells determine the velocity of excitation spread in different regions of the heart. In the SA node, cell–cell coupling is mediated by Cx30.2 and Cx45, which form low-conductance (approximately 9 and 32 pS, respectively) GJ channels. In contrast, the working cardiomyocytes of atria and ventricles express mainly Cx40 and Cx43, which form GJ channels of high conductance (approximately 180 and 115 pS, respectively) that facilitate the fast conduction necessary for efficient mechanical contraction. In the AV node, cell–cell coupling is mediated by abundantly expressed Cx30.2 and Cx45 and Cx40, which is expressed to a lesser extent. Cx30.2 and Cx45 may determine higher intercellular resistance and slower conduction in the SA- and AV-nodal regions than in the ventricular conduction system or the atrial and ventricular working myocardium. Cx30.2 and its putative human ortholog, Cx31.9, under physiologic conditions form unapposed hemichannels in nonjunctional plasma membrane; these hemichannels have a conductance of approximately 20 pS and are permeable to cationic dyes up to approximately 400 Da in molecular mass. Genetic ablation of Cxs confirmed that Cx40 and Cx43 are important in determining the high conduction velocities in atria and ventricles, whereas the deletion of the Cx30.2 complementary DNA led to accelerated conduction in the AV node and reduced the Wenckebach Period. We suggest that these effects are caused by (1) a dominant-negative effect of Cx30.2 on junctional conductance via formation of low-conductance homotypic and heterotypic GJ channels, and (2) open Cx30.2 hemichannels in non-junctional membranes, which shorten the space constant and depolarize the excitable membrane.
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Cardiac conduction abnormalities in mice lacking the gap junction protein connexin40.
Journal of cardiovascular electrophysiology, 1999Co-Authors: Sander Verheule, Klaus Willecke, C. A. J. A. C. Van Batenburg, F. E. J. Coenjaerts, Susanne Kirchhoff, Habo J. JongsmaAbstract:Cardiac Conduction in C×40−/− Mice. Introduction: The gap junction protein connexin40 (C×40) normally is expressed in the murine atrial myocardium and ventricular conduction system. In mice lacking C×40, several changes in the surface ECG have been described. In this study, we analyzed cardiac conduction in more detail. Methods and Results: In open chest mice under urethane anesthesia, epicardial electrodes were used to determine a number of atrial and ventricular pacing parameters. The corrected sinus node recovery time was significantly longer in C×40−/− mice than in C×40+/+ mice (44.4 ± 7.2 msec vs 35.5 ± 8.0 msec). In addition, the Wenckebach Period was longer in C×40−/− mice compared with the wild type (84.6 ± 5.4 msec vs 78.8 ± 3.6 msec), with the AV node probably limiting AV conduction in both cases. Whereas arrhythmias could not be induced by ventricular burst pacing in any of the mice, atrial burst pacing induced atrial tachyarrhythmias in 5 of 10 C×40−/− mice, but not in any of 9 Cx40−/− mice. Conduction velocities were measured in vivo using an array of unipolar recording electrodes. Ventricular conduction velocity did not differ between the groups, but atrial conduction velocity was reduced by 30% in C×40−/− mice compared with the wild type. Heterozygous C×40+/− mice did not differ significantly from the wild type in any respect. Conclusion: These findings indicate that in the atria and the AV conduction system, C×40 is an important determinant of conduction.
Agustin Castellanos - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms and dynamics of episodes of progression of 2:1 atrioventricular block in patients with documented two-level conduction disturbances.
American Journal of Cardiology, 1992Co-Authors: Agustin Castellanos, Alberto Interian, Manuel Mayor, Tomas Ravina, Pedro Fernández, Robert J. MyerburgAbstract:Abstract Twenty episodes of progression of 2:1 atrioventricular (AV) block were identified during incremental atrial stimulation in 7 patients with documented (2-level) block in the AV node and His-Purkinje system. All occurred at cycle lengths shorter than those at which stable 2:1 HV block had been detected. Thirteen episodes were typical since 2:1 increased to 3:1 AV Mock when an atrio-His (AH) Wenckebach Period was completed with an atrial impulse that otherwise would have been conducted. These episodes occurred with dynamic A(M): V(N) ratios similar to those seen at the AV node. Seven atypical episodes were identified (while AH Wenckebach Periods were occurring): (1) 2:1 increasing to 3:1 AV block and then to 4:1 AV block resulting from prolonged refractoriness in the His-Purkinje system subsequently followed by concealed conduction in the latter structure; (2) conversion of 3:2 directly into 3:1 AV block due to block of the next-to-last atrial impulse in the His-Purkinje system with completion of AH Wenckebach Period with the following atrial impulse; and (3) 4:2 AV block presumably due to supernormal conduction in a transversely dissociated His-Purkinje system. These episodes occurred with A(M): V(N) ratios, which in other structures would have been indicative of different degrees of AV block. In conclusion, progression of 2:1 AV block during documented 2 level conduction disturbances (1) can be explained by mechanisms different than those currently known, and (2) has rich, but different dynamics from those observed exclusively in the AV node and exclusively in the His-Purkinje system.
Alberto Interian - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms and dynamics of episodes of progression of 2:1 atrioventricular block in patients with documented two-level conduction disturbances.
American Journal of Cardiology, 1992Co-Authors: Agustin Castellanos, Alberto Interian, Manuel Mayor, Tomas Ravina, Pedro Fernández, Robert J. MyerburgAbstract:Abstract Twenty episodes of progression of 2:1 atrioventricular (AV) block were identified during incremental atrial stimulation in 7 patients with documented (2-level) block in the AV node and His-Purkinje system. All occurred at cycle lengths shorter than those at which stable 2:1 HV block had been detected. Thirteen episodes were typical since 2:1 increased to 3:1 AV Mock when an atrio-His (AH) Wenckebach Period was completed with an atrial impulse that otherwise would have been conducted. These episodes occurred with dynamic A(M): V(N) ratios similar to those seen at the AV node. Seven atypical episodes were identified (while AH Wenckebach Periods were occurring): (1) 2:1 increasing to 3:1 AV block and then to 4:1 AV block resulting from prolonged refractoriness in the His-Purkinje system subsequently followed by concealed conduction in the latter structure; (2) conversion of 3:2 directly into 3:1 AV block due to block of the next-to-last atrial impulse in the His-Purkinje system with completion of AH Wenckebach Period with the following atrial impulse; and (3) 4:2 AV block presumably due to supernormal conduction in a transversely dissociated His-Purkinje system. These episodes occurred with A(M): V(N) ratios, which in other structures would have been indicative of different degrees of AV block. In conclusion, progression of 2:1 AV block during documented 2 level conduction disturbances (1) can be explained by mechanisms different than those currently known, and (2) has rich, but different dynamics from those observed exclusively in the AV node and exclusively in the His-Purkinje system.