The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Characterization of Conduction in the Ventricles of Normal and Heterozygous Cx43 Knockout Mice Using Optical Mapping
Abstract
Conduction in Normal and C×43+/− Mice. Introduction: Gap junction channels are important determinants of conduction in the heart and may play a central role in the development of lethal cardiac arrhythmias. The recent development of a C×43‐deficient mouse has raised fundamental questions about the role of specific connexin isoforms in intercellular communication in the heart. Although a homozygous null mutation of the C×43 gene (C×43−/−) is lethal, the heterozygous (Cx43+/−) animals survive to adulthood. Reports on the cardiac electrophysiologic phenotype of the C×43+/− mice are contradictory. Thus, the effects of a null mutation of a single C×43 allele require reevaluation. Methods and Results: High‐resolution video mapping techniques were used to study propagation in hearts from C×43+/− and littermate control (C×43+/+) mice. Local conduction velocities (CVs) and conduction patterns were quantitatively measured by determining conduction vectors. We undertook the characterization of ECG parameters and epicardial CVs of normal and Cx43+/− mouse hearts. ECG measurements obtained from 12 C×43+/+ and 6 C×43+/− age matched mice did not show differences in any parameter, including QRS duration (14.5 ± 0.9 and 15.7 ± 2.3 msec for C×43+/+ and C×43+/−, respectively). In addition, using a sensitive method of detecting changes in local CV, video images of epicardial wave propagation revealed similar activation patterns and velocities in both groups of mice. Conclusion: A sensitive method that accurately measures local CVs throughout the ventricles revealed no changes in C×43+/− mice, which is consistent with the demonstration that ECG parameter values in the heterozygous mice are the same as those in wild‐type mice.
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Cites
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Self-citationCardiac Malformation in Neonatal Mice Lacking Connexin43
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Self-citationReduced cardiac conduction velocity and predisposition to arrhythmias in connexin40-deficient mice
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Slow ventricular conduction in mice heterozygous for a connexin43 null mutation.
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Cited by
Nielsen, M. S., Nygaard Axelsen, L., Sorgen, P. L., Verma, V., Delmar, M., & Holstein‐Rathlou, N. (2012) · Comprehensive Physiology · doi:10.1002/cphy.c110051 · Cited by 386
Self-citationMechanisms Underlying Conduction Slowing and Arrhythmogenesis in Nonischemic Dilated Cardiomyopathy
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Arrhythmogenic Mechanisms in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia
Cerrone, M., Noujaim, S. F., Tolkacheva, E. G., Talkachou, A., O’Connell, R., Berenfeld, O., Anumonwo, J., Pandit, S. V., Vikstrom, K., Napolitano, C., et al. (2007) · Circulation Research · doi:10.1161/circresaha.107.148064 · Cited by 285
Self-citationLi, J., Patel, V. V., Kostetskii, I., Xiong, Y., Chu, A. F., Jacobson, J. T., Yu, C., Morley, G. E., Molkentin, J. D., & Radice, G. L. (2005) · Circulation Research · doi:10.1161/01.res.0000181132.11393.18 · Cited by 223
Self-citationZhang, J., Tao, R., Campbell, K. F., Carvalho, J. L., Ruiz, E. C., Kim, G. C., Schmuck, E. G., Raval, A. N., da Rocha, A. M., Herron, T. J., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-09831-5 · Cited by 201
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Metadata
- Authors
- MORLEY, G. E., VAIDYA, D., SAMIE, F. H., LO, C., DELMAR, M., & JALIFE, J.
- Venue
- Journal of Cardiovascular Electrophysiology
- Publisher
- Wiley
- Published
- 1999-10
- Volume
- 10
- Issue
- 10
- Pages
- 1361-1375
- ISSN
- 1045-3873 (ISSN-L)
- 1540-8167
- OpenAlex
- W1993471474
- Cited by
- 269
- References
- 34
- FWCI
- 9.28
- Type
- journal article
- Language
- en
- Open access
- closed
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- MORLEY, G. E., VAIDYA, D., SAMIE, F. H., LO, C., DELMAR, M., & JALIFE, J. (1999). Characterization of Conduction in the Ventricles of Normal and Heterozygous Cx43 Knockout Mice Using Optical Mapping. Journal of Cardiovascular Electrophysiology. https://doi.org/10.1111/j.1540-8167.1999.tb00192.x
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