Defibrotide Limits Heart Damage in Cats During Induced Heart Attacks

Niada and colleagues, writing in Thrombosis Research in 1985, studied defibrotide — a natural polydeoxyribonucleotide (a chain of DNA building blocks) — in cats experiencing an artificially induced heart attack. This is an animal pharmacology study, not a human trial, and it looks at defibrotide as a circulatory drug rather than as a skin or regenerative ingredient.

The researchers tied off a coronary artery in anesthetized cats to cut blood flow to part of the heart, then gave some animals defibrotide intravenously (32 mg per kg per hour) for the full five hours of blocked blood flow. Compared with untreated ischemia, defibrotide reduced the ECG changes (ST-segment rises) linked to heart damage, improved a measure of heart pumping performance called the pressure-rate index, and prevented the ischemia-induced changes in lactate, ATP and the enzyme CPK in the affected heart tissue. A comparison drug, prostacyclin (PGI2), produced similar effects; a beta-blocker, atenolol, protected CPK levels but not lactate or ATP.

The authors suggest defibrotide may work partly by boosting the body's own prostacyclin release and by reducing platelet clumping, improving local oxygen and energy supply. The study cannot show whether these effects occur in humans, nor does it address any role for polydeoxyribonucleotides in skin or wound healing.