Furazolidone-Induced Cardiomyopathy: Biomedical Model for the Study of Cardiac Hypertrophy and Congestive Heart Failure

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Abstract
A developmental morphologic study was undertaken to identify the sequence of myocardial ultrastructural changes during the production of furazolidone-induced cardiomyopathy in turkey poults 3-5 wk posthatching. Morphologic changes commonly associated with cardiac hypertrophy were observed. These changes provided a basis for formulation of a hypothesis describing the sequential events responsible for the development of drug-induced cardiomyopathy. It is postulated that the drug''s initial effects occur in the membrane systems of the myocardial cell. This may be due to enzyme inhibition that leads to alteration of the mitochondrial and myofibrillar components with a concomitant increase in cytoplasmic glycogen. Hypertrophy is the consequence of the cell''s compensatory response to the injurious effects of the drug. The basis for this working hypothesis is discussed. Number, sequence and severity of morphologic changes indicate that the avian round-heart syndrome is an appropriate model system for studying biochemical and degenerative processes during the development of drug-induced cardiac hypertrophy.

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