Technical Abstract: Adonis aestavalis (pheasant’s eye) is an introduced European species that contains several cardenolides including adonitoxin, cymarin, K-strophanthin, and vernadigin. These cardenolides, more potent than digitoxin, produce similar positive inotropic effects by inhibiting membrane bound Na-K ATPase. Since pheasant’s eye is not highly palatable, most poisonings are caused by contaminated hay. In field poisoning animals often die with minimal or non-apparent gross or histologic lesions. The purpose of this study was to verify Adonis toxicity in a rodent model and document the histologic and ultrastructural lesions of poisoning. Adonis aestavalis was collected, frozen, freeze dried, finely ground, and dosed to 3 groups of 10 Syrian hamsters at a rate of 0, 100 and 200 mg/kg QID for 7 days. High dose animals developed diarrhea, anorexia and became reluctant to move. Histologically the myocardial lesions were subtle with focal myocyte swelling and vacuolation. Ultrastructrually there were early lesions of mitochondrial swelling and myofiber disruption. These findings indicated the Adonis aestavalis is toxic and myocardial lesions typical of cardioglycoside poisoning may be minimal. The production of the classical cardioglycoside-associated myocardial lesions is variable and it is probably related to dose, duration, and recovery time.