We have previously demonstrated that turkey poults fed
furazolidone (Fz) in high concentrations (700 ppm) develop
dilated cardiomyopathy (DCM) which approximates the human condition [1-3]. We wanted to study the effects of a
calcium channel blocker in an animal model with a documented decrease in beta-receptor density, increased levels of circulating
catecholamines, and abnormal
calcium metabolism. The effects of a third generation
calcium channel blocker has not been studied in our model. We hypothesized that the model would be predictive of the human condition and provide additional insights into the potential use of Ca2+ channel blockers in the setting of DCM. In the present study, we examined the effect of
pranidipine, a new
dihydropyridine calcium antagonist, in the setting of DCM on the gross and microscopic morphology of the heart and the overall contractile performance of the myocardium. A state of symptomatic to mild
cardiomyopathy was induced in Broad-Breasted White turkey poults by administration of Fz for three weeks. Blood pressure, heart rate, fractional shortening, and
body weight were monitored and compared in DCM animals treated with
pranidipine and those given a placebo. After four weeks of treatment or no treatment with
pranidipine, animals were euthanized and heart weight, cardiac dimensions, and microscopic morphology were compared. Progressive left ventricular (LV) dilatation and wall thinning was prevented with
pranidipine treatment. In addition, microscopic examination demonstrated myocyte
hypertrophy regression in DCM animals treated with
pranidipine. In DCM animals, treatment with
pranidipine resulted in significantly smaller left ventricular dimensions. We conclude that the
calcium channel blocker pranidipine was not detrimental to global cardiac function in animals with
dilated cardiomyopathy.