Defibrotide Shields Cat Heart Tissue from Reperfusion Injury

Thiemermann and colleagues, writing in The American Journal of Cardiology in 1985, studied defibrotide, a partially broken-down polydeoxyribonucleotide taken from mammalian lungs, in cats whose heart blood supply was temporarily blocked. The question was whether the compound could limit damage that occurs when blood flow returns after a blocked artery — so-called reperfusion injury.

The researchers blocked a coronary artery in cats for three hours, then let blood flow return for two hours. Animals given defibrotide intravenously (a 32 mg/kg bolus followed by a 32 mg/kg/hour infusion) lost 60% less of an enzyme marker of heart muscle damage (creatine kinase activity) compared with untreated cats. Treated animals also showed less ECG change during the blockage and did not develop the abnormal Q wave seen in untreated cats during early reperfusion. Of 8 untreated cats, 2 died from an irregular heartbeat and one had severe arrhythmia; all 7 defibrotide-treated cats survived. In separate experiments, defibrotide increased release of prostacyclin, a substance that affects blood vessel and clotting activity, by 8- to 10-fold, which the authors suggest may explain part of the protective effect.

This is an animal study in cats only, using a specific lung-derived compound, and cannot establish effects in humans or in skin or wound contexts.