Hostname: page-component-77c89778f8-n9wrp Total loading time: 0 Render date: 2024-07-17T11:37:01.105Z Has data issue: false hasContentIssue false
  • English
  • Français

The Syrian Golden Hamster: A Model for the Cardiomyopathy of Friedreich's Ataxia

Published online by Cambridge University Press:  18 September 2015

J. Azari ,
T. Reisine ,
A. Barbeau ,
H.I. Yamamura  and
R. Huxtable
J. Azari
Affiliation:
Department of Pharmacology, University of Arizona Health Sciences Center, Tucson and the Department of Neurobiology, Clinical Research Institute of Montreal
T. Reisine
Affiliation:
Department of Pharmacology, University of Arizona Health Sciences Center, Tucson and the Department of Neurobiology, Clinical Research Institute of Montreal
A. Barbeau
Affiliation:
Department of Pharmacology, University of Arizona Health Sciences Center, Tucson and the Department of Neurobiology, Clinical Research Institute of Montreal
H.I. Yamamura
Affiliation:
Department of Pharmacology, University of Arizona Health Sciences Center, Tucson and the Department of Neurobiology, Clinical Research Institute of Montreal
R. Huxtable
Affiliation:
Department of Pharmacology, University of Arizona Health Sciences Center, Tucson and the Department of Neurobiology, Clinical Research Institute of Montreal
Rights & Permissions [Opens in a new window]

Summary

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

In light of the available information on the cardiomyopathy of Friedreich's ataxia, the cardiomyopathic Syrian hamster may be an appropriate laboratory model. Cardiomyopathy in these animals is a result of calcium accumulation. We analyzed the atria and right and left ventricles from cardiomyopathic (CM) and random bred (RB) animals for calcium, magnesium, and iron concentrations at 30-40 and 60-70 days of age (age of maximum lesioning). There are no significant differences in the concentration of iron or magnesium among age-matched groups. The concentration of calcium in the left ventricles of the CM animals at 60 days old is 14 fold higher than that of R B animals. Although there is a significant difference in the concentration of calcium in the left ventricles of younger animals, it is not as pronounced as the difference in older animals. Analysis of the taurine concentration in 30-40 day old animals revealed that the CM animals show slightly higher taurine concentrations than RB in the whole heart. In 60 day old CM hamsters the ß-adrenergic receptor density of the ventricles is unchanged. This indicates that calcium overload is not due to a drene rg i c super sensitivity.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 6 , Issue 2 , May 1979 , pp. 223 - 226
Copyright
Copyright © Canadian Neurological Sciences Federation 1979

References

Bajusz, E., Baker, J. R., Nixon, C. W. and Hamburger, F. (1969). Spontaneous hereditary myocardial degeneration and congestive heart failure in the Syrian hamster. Annals of New York Academy of Sciences 156 105–129.Google Scholar
Bylund, D. and Snyder, S. (1976). ß-Adrenergic receptor binding in membrane preparations from mammalian brain. Mol. Pharm. 12 568–580.Google Scholar
Chubb, J. and Huxtable, R. (1978). Transport and biosynthesis of taurine in the stressed hearts.In “Taurine and Neurological Disorders,” Barbeau, A. and Huxtable, R., Eds., pp 161–178. Raven Press, New York.Google Scholar
Dolara, P., Agresti, A., Giotti, A. and Pasquini, G. (1973). Effect of taurine on calcium kinetics of guinea pig heart. Eur. J. Pharmacol. 24 352–358.Google ScholarPubMed
Fleckenstein, A. (1971). Specific inhibitors and promotors of calcium action in the excitation contraction coupling of heart muscle and their role in prevention or production of myocardial lesions. In “Calcium and the Heart,” P., Harris and L., Opie, Eds., pp 135–188. Academic Press, London.Google Scholar
Fleckenstein, A., Janke, J.Döring, H. J. and Leder, O. (1974). Myocardial fiber necrosis due to intracellular calcium overload. In “Myocardial Biology,” Dhalla, N.S., Ed., pp 563–580. University Park Press, Baltimore.Google Scholar
Fleckenstein, A., Janke, J., Döring, H. J. and Leder, O. (1975). Key role of calcium in the production of non-coronogenic myocardial necrosis. In “Pathophysiology and Morphology of Myocardial Cell Alterations,” Fleckenstein, A. and Rona, G., Eds. , pp 21–32. University Park Press, Baltimore.Google Scholar
Goldman, H. and Scriver, C. R. (1967). A transport system in mammalian kidney with preference for β-amino acid compounds. Ped. Res. 1 212–213.Google Scholar
Hartman, J. W. and Booth, R. W. (1960). Friedreich's ataxia: A neurocardiac disease. Amer. Heart J. 60 716–720.Google ScholarPubMed
Hruška, R. E., Huxtable, R. J. and Yamamura, H. I. (1978). High affinity temperature-sensitive, and sodium dependent transport of taurine in rat brain. In “Taurine and Neurological Disorders,” Barbeau, A. and Huxtable, R., Eds., pp 109–117. Raven Press, New York.Google Scholar
Huxtable, R. (1978). Cardiac pharmacology and cardiomyopathy in Friedreich's ataxia. Can. J. Neurol. Sci. 5 83–91.Google ScholarPubMed
Huxtable, R. and Bressler, R. (1973). Effect of taurine on a muscle intracellular membrane. Biochem. Biophys. Acta 323 573–583.Google ScholarPubMed
Huxtable, R. and Bressler, R. (1974). Elevation of taurine in human congestive heart failure. Life Sciences 14 1353–1359.Google ScholarPubMed
Huxtable, R. and Chubb, J. (1976). Taurine and isoproterenol toxicity. Proc. West. Pharmacol. Soc. 19 316–319.Google ScholarPubMed
Lossnitzer, K. and Bajusz, E. (1973). Electrolyte and water alteration during the life course of the Bio 14.6 Syrian golden hamster representing a disease model of a hereditary cardiomyopathy.In “Card io myopathies,” Bajusz, E. and Rona, G., Eds., pp 503–505. University Park Press, Baltimore.Google Scholar
Lowry, O., Rosebrough, N., Farr, A. and Randall, R. (1951). Protein measurement with folin phenol reagent. J. Biol. Chem. 193 265–275.Google ScholarPubMed
Malo, S., Latour, Y., Coté, M., Geoffroy, G., Lemieux, B. and Barbeau, A. (1976). Electrocardiogra-phic and vectrocardiographic findings in Friedreich's ataxia. Can. J. Neurol. Sci. 3 323–328.Google Scholar
Sanchez-Casis, G., Coté, M. and Barbeau, A. (1976). Pathology of the heart in Friedreich's ataxia: Review of the literature and report of one case. Can. J. Neurol. Sci. 3 349–354.Google ScholarPubMed
Schwartz, A., Sordahl, L., Crow, C., McCollum, W., Harigaya, S. and Bajusz, E. (1972). Several biochemical characteristics of the cardiomyopathic Syrian hamster. In “Myocardiology,” Bajusz, E. and Rona, G., Eds. , pp 235–242. University Park Press, Baltimore.Google ScholarPubMed