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헤파린 MSDS

• Heparin

헤파린 화학적 특성, 용도, 생산

• 개요

  Parnaparin sodium is a low molecular weight heparin obtained from bovine mucosal heparin by chemical depolymerization. It has more potent antithrombotic and profibrinolytic activity than heparin evidenced by its higher activity in inhibiting factor Xa and in reducing plasma activity of platelet activator inhibitor. It is effective in improving the venous blood outflow of lower limbs in deep vein thrombosis (DVT) patients in addition to preventing DVT following orthopaedic surgery, reportedly without causing bleeding complications. Parnaparin has also shown efficacy in inflammatory occlusive complications of postphlebitic syndrome and in acute myocardial infarction.

• 화학적 성질

  White or pale-colored amorphous powder; nearly odorless; hygroscopic. Soluble in water; insoluble in alcohol, benzene, acetone, chloroform, and ether; pH in 17% solution between 5.0 and 7.5.

• 출처

  Heparin is a complex organic acid (mucopolysaccharide) present in mammalian tissues and a strong inhibitor of blood coagulation. Although the precise formula and structure of heparin are uncertain, it has been suggested that the formula for sodium heparinate, generally the form of the drug used in anticoagulant therapy, is (C12H16N2Na3)20 with a molecular weight of about 12,000. The commercial drug is derived from animal livers or lungs.

• 용도

  Medicine (anticoagulant), biochemical research, rodenticides.

• 정의

  heparin: A glycosaminoglycan (mucopolysaccharide)with anticoagulantproperties, occurring in vertebratetissues, especially the lungs andblood vessels.

• Biological Functions

  Heparin (heparin sodium) is a mixture of highly electronegative acidic mucopolysaccharides that contain numerous N- and O-sulfate linkages. It is produced by and can be released from mast cells and is abundant in liver, lungs, and intestines.

• 위험도

  May cause internal bleeding.

• Mechanism of action

  The anticoagulation action of heparin depends on the presence of a specific serine protease inhibitor (serpin) of thrombin, antithrombin III, in normal blood.
  Heparin binds to antithrombin III and induces a conformational change that accelerates the interaction of antithrombin III with the coagulation factors. Heparin also catalyzes the inhibition of thrombin by heparin cofactor II, a circulating inhibitor. Smaller amounts of heparin are needed to prevent the formation of free thrombin than are needed to inhibit the protease activity of clot-bound thrombin. Inhibition of free thrombin is the basis of low-dose prophylactic therapy.

• Pharmacokinetics

  The pharmacokinetic profiles of heparin and LMWHs are quite different. Whereas heparin is only 30% absorbed following subcutaneous injection, 90% of LMWH is systemically absorbed. The binding affinity of heparin to various protein receptors, such as those on plasma proteins, endothelial cells, platelets, platelet factor 4 (PF4), and macrophages, is very high and is related to the high negative-charged density of heparin. This high nonspecific binding decreases bioavailability and patient variability. Additionally, heparin's nonspecific binding may account for heparin's narrow therapeutic window and heparin-induced thrombocytopenia (HIT), a major limitation of heparin. These same affinities are quite low, however, in the case of LMWHs. These parameters explain several of the benefits of the LMWH's. The favorable absorption kinetics and low protein binding affinity of the LMWHs results in a greater bioavailability compared with heparin. The lowered affinity of LMWHs for PF4 seems to correlate with a reduced incidence of HIT. Heparin is subject to fast zero-order metabolism in the liver, followed by slower first-order clearance from the kidneys. The LMWHs are renally cleared and follow first-order kinetics. This makes the clearance of LMWHs more predictable as well as resulting in a prolonged half-life. Finally, the incidence of heparin-mediated osteoporosis is significantly diminished with use of LMWHs as opposed to heparin.

• Pharmacology

  The physiological function of heparin is not completely understood. It is found only in trace amounts in normal circulating blood. It exerts an antilipemic effect by releasing lipoprotein lipase from endothelial cells; heparinlike proteoglycans produced by endothelial cells have anticoagulant activity. Heparin decreases platelet and inflammatory cell adhesiveness to endothelial cells, reduces the release of platelet-derived growth factor, inhibits tumor cell metastasis, and exerts an antiproliferative effect on several types of smooth muscle.
  Therapy with heparin occurs in an inpatient setting. Heparin inhibits both in vitro and in vivo clotting of blood. Whole blood clotting time and activated partial thromboplastin time (aPTT) are prolonged in proportion to blood heparin concentrations.

• 부작용

  The major adverse reaction resulting from heparin therapy is hemorrhage. Bleeding can occur in the urinary or gastrointestinal tract and in the adrenal gland. Subdural hematoma, acute hemorrhagic pancreatitis, hemarthrosis, and wound ecchymosis also occur. The incidence of life-threatening hemorrhage is low but variable. Heparin-induced thrombocytopenia of immediate and delayed onset may occur in 3 to 30% of patients. The immediate type is transient and may not involve platelet destruction, while the delayed reaction involves the production of heparin-dependent antiplatelet antibodies and the clearance of platelets from the blood. Heparin-associated thrombocytopenia may be associated with irreversible aggregation of platelets (white clot syndrome). Additional untoward effects of heparin treatment include hypersensitivity reactions (e.g., rash, urticaria, pruritus), fever, alopecia, hypoaldosteronism, osteoporosis, and osteoalgia.

• 신진 대사

  Heparin is prescribed on a unit (IU) rather than milligram basis. The dose must be determined on an individual basis. Heparin is not absorbed after oral administration and therefore must be given parenterally. Intravenous administration results in an almost immediate anticoagulant effect. There is an approximate 2-hour delay in onset of drug action after subcutaneous administration. Intramuscular injection of heparin is to be avoided because of unpredictable absorption rates, local bleeding, and irritation. Heparin is not bound to plasma proteins or secreted into breast milk, and it does not cross the placenta.
  Heparin’s action is terminated by uptake and metabolism by the reticuloendothelial system and liver and by renal excretion of the unchanged drug and its depolymerized and desulfated metabolite. The relative proportion of administered drug that is excreted as unchanged heparin increases as the dose increases. Renal insufficiency reduces the rate of heparin clearance from the blood.

• Purification Methods

  Most likely contaminants are mucopolysaccharides including heparin sulfate and dermatan sulfate. Purify heparin by precipitation with cetylpyridinium chloride from saturated solutions of high ionic strength. [Cifonelli & Roden Biochemical Preparations 12 12 1968, Wolfrom et al. J Org Chem 29 540 1946, Huggard Adv Carbohydr Chem 10 336-368 1955]

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