Defibrotide Protects Rabbit Hearts From Damage After Induced Heart Attack

Berti and colleagues, writing in the Journal of Cardiovascular Pharmacology in 1986, studied defibrotide, a single-strand polydeoxyribonucleotide of mammalian origin with a molecular weight of about 20,000 daltons, in rabbits with experimentally induced heart attacks.

The researchers gave defibrotide intravenously to rabbits before and after they induced damage to the heart's left ventricle, then examined the hearts three days later in isolated, perfused preparations. Untreated infarcted hearts showed abnormal responses to adrenaline-like compounds: weaker contraction in response to isoproterenol and tyramine, but a stronger-than-normal response to phenylephrine. Rabbits pretreated with defibrotide (32 mg/kg/hour for 6 hours) largely avoided these shifts, with drug-response ratios between injured and healthy hearts coming out close to normal (near 1). A lower dose of defibrotide (8 mg/kg/hour for 6.5 hours) also prevented the usual drop in an enzyme called CPK, a marker of heart muscle damage. The authors link these effects partly to defibrotide's known ability to prevent blood clotting and promote release of a clot-dissolving substance called prostacyclin.

This is a rabbit laboratory study using one specific drug substance; it does not show effects in humans or indicate anything about skin, wound healing, or topical use.