Morphological changes associated with furazolidone-induced cardiomyopathy: effects of digoxin and propranolol.

The purpose of the present study was to examine light microscopic data qualitatively as well as quantitatively from an animal model of dilated cardiomyopathy in the turkey. A previous study reported the gross cardioprotective effect of propranolol and the lack of cardioprotection with digoxin in furazolidone-induced cardiomyopathy. It was therefore important to define whether the response of the myocardium to therapeutic interventions differed from the structural responses seen in their absence. In furazolidone-treated birds with resultant cardiac dilation there was myocyte hypertrophy, enlargement of nuclei and reorientation of subepicardial myocardial fibres. Similar changes were noted in birds receiving both furazolidone and digoxin. However, birds receiving propranolol, a non-selective beta-receptor antagonist, and furazolidone did not demonstrate a hypertrophic response or reorientation of fibres. These data indicate that propranolol maintained myocardial morphology and morphometry and thus prevented the structural sequelae of the disease, which is a better achievement of therapy than simple arrest of the progress. A role for intracellular calcium is implied. The cardioprotective effect seen with beta blockade suggests that membrane related events may lead to the contractile dysfunction that results in dilation and cardiac hypertrophy.