| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print October 17, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00546.2002
Submitted on July 2, 2002
Accepted on September 28, 2002
1 Department of Medicine, University of Calgary, Calgary, Alberta, Canada
2 Department of Pharmacology and Therapeutics, University of Calgary, Calgary, Alberta, Canada
3 Department of Molecular Cardiovascular Biology, Children's Hospital Medical Center, Cincinnati, Ohio, USA
* To whom correspondence should be addressed. E-mail: hduff{at}ucalgary.ca.
Objectives: Echocardiograms have been assessed only at 56 days in mice overexpressing calcineurin (CN). Age-dependent echocardiographic changes were evaluated because development of sudden death is time-dependent. Since cyclosporin A (CsA) reverses hypertrophy in CN mice, its effects on the time-course of development of sudden death and cardiac dysfunction were assessed. Methods and Results: In wildtype mice (WT), left ventricular internal end-diastolic dimension (LVIDd) increased and left ventricular mass index (LVMI) decreased with age. In CN, two distinct phases of pathophysiology were found. At 14 days in CN, LVIDd and LVMI were significantly increased but sudden death had not occurred. After 28 days, relative dilation of the CN left ventricle occurred while LVMI decreased. Sudden death developed during progressive dilation associated with systolic and diastolic dysfunction. CsA treatment reversed hypertrophy in CN mice but did not reverse systolic and diastolic dysfunction and exaggerated sudden death. Conclusion: Sudden cardiac death was associated with systolic and diastolic dysfunction but was not related to isolated cardiac hypertrophy in CN mice.
This article has been cited by other articles:
|
|
 |
|
  R. J. Gelpi, S. Gao, P. Zhai, L. Yan, C. Hong, L. M. A. Danridge, H. Ge, Y. Maejima, M. Donato, M. Yokota, et al. Genetic inhibition of calcineurin induces diastolic dysfunction in mice with chronic pressure overload Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1814 - H1819. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. MacDonnell, J. Weisser-Thomas, H. Kubo, M. Hanscome, Q. Liu, N. Jaleel, R. Berretta, X. Chen, J. H. Brown, A.-K. Sabri, et al. CaMKII Negatively Regulates Calcineurin-NFAT Signaling in Cardiac Myocytes Circ. Res., August 14, 2009; 105(4): 316 - 325. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Espinoza-Derout, M. Wagner, L. Salciccioli, J. M. Lazar, S. Bhaduri, E. Mascareno, B. Chaqour, and M.A.Q. Siddiqui Positive Transcription Elongation Factor b Activity in Compensatory Myocardial Hypertrophy is Regulated by Cardiac Lineage Protein-1 Circ. Res., June 19, 2009; 104(12): 1347 - 1354. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Stypmann, M. A Engelen, C. Troatz, M. Rothenburger, L. Eckardt, and K. Tiemann Echocardiographic assessment of global left ventricular function in mice Lab Anim, April 1, 2009; 43(2): 127 - 137. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. Somers, P. L. Beck, J. P. Lees-Miller, D. Roach, Y. Li, J. Guo, S. Loken, S. Zhan, L. Semeniuk, and H. J. Duff iNOS in cardiac myocytes plays a critical role in death in a murine model of hypertrophy induced by calcineurin Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1122 - H1131. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Pinz, S. E. Ostroy, K. Hoyer, H. Osinska, J. Robbins, J. D. Molkentin, and J. S. Ingwall Calcineurin-induced energy wasting in a transgenic mouse model of heart failure Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1459 - H1466. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Zhao, N. H. Jeoung, S. C. Burgess, K. A. Rosaaen-Stowe, T. Inagaki, S. Latif, J. M. Shelton, J. McAnally, R. Bassel-Duby, R. A. Harris, et al. Overexpression of pyruvate dehydrogenase kinase 4 in heart perturbs metabolism and exacerbates calcineurin-induced cardiomyopathy Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H936 - H943. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Suzuki, E. Bayna, H. L. Li, E. D. Molle, and W. Y.W. Lew Lipopolysaccharide Activates Calcineurin in Ventricular Myocytes J. Am. Coll. Cardiol., January 30, 2007; 49(4): 491 - 499. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Guo, S. Zhan, J. Somers, R. E. Westenbroek, W. A. Catterall, D. E. Roach, R. S. Sheldon, J. P. Lees-Miller, P. Li, Y. Shimoni, et al. Decrease in density of INa is in the common final pathway to heart block in murine hearts overexpressing calcineurin Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2669 - H2679. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Funakoshi, T. O. Chan, J. C. Good, J. R. Libonati, J. Piuhola, X. Chen, S. M. MacDonnell, L. L. Lee, D. E. Herrmann, J. Zhang, et al. Regulated Overexpression of the A1-Adenosine Receptor in Mice Results in Adverse but Reversible Changes in Cardiac Morphology and Function Circulation, November 21, 2006; 114(21): 2240 - 2250. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. S.C. Khoo, J. Li, M. V. Singh, Y. Yang, P. Kannankeril, Y. Wu, C. E. Grueter, X. Guan, C. V. Oddis, R. Zhang, et al. Death, Cardiac Dysfunction, and Arrhythmias Are Increased by Calmodulin Kinase II in Calcineurin Cardiomyopathy Circulation, September 26, 2006; 114(13): 1352 - 1359. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Zhang, G. Azhar, M. C. Furr, Y. Zhong, and J. Y. Wei Model of functional cardiac aging: young adult mice with mild overexpression of serum response factor Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2003; 285(3): R552 - R560. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
