Cardiomyocyte Calcium Transients in German Shepherd Dogs with Inherited Ventricular Arrhythmias
ACVIM 2008
S.A. Jesty1; B.G. Kornreich1; J. Cordeiro2; C. Antzelevitch2; N.S. Moïse1
1College of Veterinary Medicine, Cornell University, Ithaca, NY, USA; 2Masonic Medical Research Laboratory, Utica, NY, USA


Inherited ventricular arrhythmias and abnormalities of repolarization have been documented in German shepherd dogs (GSDs). The purpose of this study was to determine the temporospatial aspects of calcium cycling in the ventricular cells of affected GSDs and normal dogs. The hypotheses were that calcium transients in the ventricular cells of affected GSDs would be different from those in normal dogs; and that calcium sparks and early/delayed after depolarizations (EADs/DADs) would be more numerous in cells of affected dogs as a result of the calcium cycling abnormalities.

Ten affected GSDs and 10 unaffected dogs were studied. Midmyocardial cells (M cells) were harvested from dogs after euthanasia. Myocytes were loaded with Fluo 3, a fluorophore whose emission spectrum is shifted in the presence of calcium. Myocytes were field stimulated and XT line scan images were recorded using confocal microscopy.

M cells from affected GSDs displayed a high variation in the decay phase of the calcium transient (Tau), compared with normal dogs (Figure). Affected dogs had a mixture of abnormal and normal cells, whereas normal dogs had more consistent calcium cycling across cells. Additionally, the number of calcium sparks, EADs, and DADs was greater in affected GSDs.

These results indicate that abnormalities of calcium cycling, and specifically cell to cell electrical heterogeneity, may be a mechanism contributing to the inherited ventricular arrhythmias in GSDs.

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Sophy Jesty

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