Heparin, which was discovered by McLean in 1916, has been used widely for anticoagulation. The predominant mode of action is potentiation of naturally occurring antithrombin III, although platelets and proteins in the cell wall are also affected. Unfractionated heparin reduces the adhesion of platelets to injured arterial walls, probably by maintaining vessel-wall electronegativity. Heparin also binds to platelets and promotes in vitro aggregation. In contrast, heparin has been shown to reduce platelet aggregation to collagen.

Heparin is known to increase clotting time by affecting several coagulation factors simultaneously, leading to occult blood loss and hemorrhagic complications. Inhibition of b-factor XIIa by C1 inhibitor is reduced by heparin and varies depending on heparin type. Therefore heparins may potentiate contact activation.

The half-life of heparin is known to be dose dependent and increases with prolonged administration.

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Sleep Apnea

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