Why the study?
Does long-term dipyridamole treatment reduce myocardial hypertrophy and improve cardiac contractility in aorta-stenosed growing rabbits?
Does long-term dipyridamole treatment reduce myocardial hypertrophy and improve cardiac contractility in aorta-stenosed growing rabbits?
Long-term dipyridamole treatment may retard myocardial hypertrophy and preserve cardiac contractility in a rabbit model of aortic stenosis.
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Hypothesis-generating in rabbit aortic stenosis; leaves open any clinical translation of dipyridamole.
The well-known effects of dipyridamole on the increase of the coronary vessel system and on cardiac metabolism suggest that dipyridamole may have a favourable influence on the chronic pressure loaded heart. In the model of the aorta-stenosed growing rabbit the cardiomegaly was diminished after a 3-month treatment using high doses of dipyridamole. Histometrically a marked decrease of the enlargement of the cross-sectional area of muscle fibres was found. It is assumed that dipyridamole retards myocardial hypertrophy and stimulates hyperplasia. Simultaneously the impairment of distinct parameters of cardiac contractility in the aorta-stenosed heart was prevented in growing rabbits by long-term dipyridamole treatment.
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BLASS et al. (1976) studied this question.
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