Abstract

Heparin’s obscure endogenous function may be resolved by new experimental findings, reported by Saliba and coworker since 1963, with heparin use in controlled animal studies and patients with thermal burns and myocardial ischemia. Large doses of intestinal source heparin, administered topically and parenterally, significantly reduced burn extension, edema, fasciectcmies, parenteral fluids, skin grafts, and contractures. Then, similar large doses of intestinal source heparin significantly reduced the cellular-destructive pathophysiology of myocardial ischemia, improved electrocardiographic S-T segments 84%, reduced myocardial necrosis 32%, and salvaged creatine Phosphokinase 15%. Lung source heparin produced significant but lesser effects on S-T segment elevations and adenosine triphosphate levels. The large heparin dose needs, without bleeding problems, suggested more than anticoagulation was involved. Ml known heparin effects were theoretical mechanisms: anticoagulant, antithrombosis, antilipemia, antihistamine, anti-serotonin, antiproteolytic enzyme, anticcmplement, antilysosomal enzyme, and antiexcess positive ion. For those effects, individually often and collectively always, large doses of heparin were required. Inactivation-combination reactions of heparin with histamrine, serotonin and some tested proteolytic enzymes were ph related, acidic ph dependent, alkaline ph reversible. So, thermal burns and myocardial infarcts were two severe cellular-destructive diseases, with ischemic components, that were significantly improved by appropriately large doses of source specific heparin. It is concluded that at acidic phs intestinal heparin in larger than anticoagulative dose is mainly an anticellular-destructive agent, incidentally anticoagulant. New uses may result.

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