Effects of pranidipine, a calcium channel antagonist, in an avian model ofheart failure

We have previously demonstrated that turkey poults fed furazolidone (Fz) in high concentrations (700 ppm) develop dilated cardiomyopathy (DCM) which a pproximates 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 be ta-receptor density, increased levels of circulating catecholamines, and ab normal calcium metabolism. The effects of a third generation calcium channe l 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 dihydropyri dine calcium antagonist, in the setting of DCM on the gross and microscopic morphology of the heart and the overall contractile performance of the myo cardium. A state of symptomatic to mild cardiomyopathy was induced in Broad -Breasted White turkey poults by administration of Fz for three weeks. Bloo d pressure, heart rate, fractional shortening, and body weight were monitor ed and compared in DCM animals treated with pranidipine and those given a p lacebo. After four weeks of treatment or no treatment with pranidipine, ani mals 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, micros copic examination demonstrated myocyte hypertrophy regression in DCM animal s treated with pranidipine. In DCM animals, treatment with pranidipine resu lted in significantly smaller left ventricular dimensions. We conclude that the calcium channel blocker pranidipine was not detrimental to global card iac function in animals with dilated cardiomyopathy.