Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Heparin platelet effects

The fibrinolytic activity of the onion and garlic constituent cyclo-alliin has been confirmed.Aspirin has been reported to have fibrinolytic activity, independent of its platelet effects. A heparin-urea complex was reported to enhance fibrinolysis, while each component separately had no effect. [Pg.77]

A number of laboratory tests are available to measure the phases of hemostasis described above. The tests include platelet count, bleeding time, activated partial thromboplastin time (aPTT or PTT), prothrombin time (PT), thrombin time (TT), concentration of fibrinogen, fibrin clot stabifity, and measurement of fibrin degradation products. The platelet count quantitates the number of platelets, and the bleeding time is an overall test of platelet function. aPTT is a measure of the intrinsic pathway and PT of the extrinsic pathway. PT is used to measure the effectiveness of oral anticoagulants such as warfarin, and aPTT is used to monitor heparin therapy. The reader is referred to a textbook of hematology for a discussion of these tests. [Pg.608]

Heparin-induced thrombocytopenia (HIT) is a very serious adverse effect associated with UFH use. Platelet counts should be monitored every 2 to 3 days dining the course of UFH therapy.5 HIT should be suspected if the platelet count drops by more than 50% from baseline or to below 120,000. In patients with contraindications to anticoagulation therapy, UFH should not be administered (Table 7-7). [Pg.146]

In practice, some anticoagulation agents such as heparin or antiplatelet agents, e.g. nitric oxide (NO) are delivered to sensor sites in order to reduce the risk of thrombus formation. Nitric oxide (NO), which is a potent inhibitor of platelet adhesion and activation as well as a promoter of wound healing in tissue, has been incorporated in various polymer metrics including PVC (poly(vinyl-chloride)), PDMS (poly-dimethyl-siloxane) and PU (poly-urethanes). Those NO release polymers have been tested in animals as outer protection coatings and have shown promising effects for the analytical response characteristics of the sensor devices [137],... [Pg.312]

The answer is d. (Hardman, p 1346.) A slow intravenous infusion of protamine sulfate will quickly reverse the bleeding. Protamine binds to heparin to form a stable complex with no anticoagulant activity It may also have its own anticoagulant effect by binding with platelets and fibrinogen. [Pg.125]

Hydrophobic polymer materials that slowly release N O can be used on the surface of medical devices. Many medical devices suffer from the surface adhesion of blood platelets. To minimize this thrombogenic effect, blood thinners such as heparin, coumarin, and aspirin are often used. However, systemic administration of antiplatelet agents could increase the risk of uncontrolled bleeding elsewhere in the body. In contrast, biocompatible polymer films would solve this problem [153]. It is possible to create polymeric surfaces that mimic the inner surface of a blood vessel by... [Pg.24]

Therapy, in the short term, is with intravenous unfractionated or subcutaneous low molecular weight heparin. Aspirin, given in low doses between 50 and 100 mg per day, is sufficient to diminish platelet-vessel interaction. Alternatives include 100-200 mg of sulphinpyrazone once or twice a day or dipyridamole where 100 mg four times a day can be used on its own or between 25 and 75 mg combined with aspirin three times a day. More recently thiopy-ridines, as a class, has been shown to have equivalence at 250 mg twice a day. In hyperhomocysteinaemia the risk is reduced by 5 mg of folate and 100 mg of vitamin Bg daily, with addition of oral vitamin Bi2 of less clearly defined benefit. The effect of this intervention requires re-assay at 3-monthly intervals, following standard methionine challenge, to ensure that suitable suppression has been achieved in the plasma amino acid level (Table 5). [Pg.745]

The physiological function of heparin is not completely understood. It is found only in trace amounts in normal circulating blood. It exerts an antihpemic effect by releasing lipoprotein lipase from endothehal 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. [Pg.259]

Drugs that inhibit platelet function (e.g., aspirin) or produce thrombocytopenia increase the risk of bleeding when heparin is administered. Oral anticoagulants and heparin produce synergistic effects. Many basic drugs precipitate in the presence of the highly acidic heparin (e.g., antihistamines, quinidine, quinine, phenothiazines, tetracycline, gentamicin, neomycin). [Pg.260]

B. Thrombocytopenia is a frequent side effect association with heparin. This reduction in the level of circulating platelets increases bleeding. Purple toes are encountered during warfarin therapy. Heparin may be administered to pregnant mothers without risk to the fetus. Heparin requires antithrombin III for its anticoagulant action, but does not increase the level of this protein in the blood. [Pg.266]

Mechanism of Action An antithrombin that inhibits factor Xa and thrombin in the presence of low-molecular-weight heparin. Only slightly influences platelet aggregation, PT, and aPTT. Therapeutic Effect Produces anticoagulation. [Pg.320]

Mechanism of Action A low-molecular-weight heparinthat inhibits factor Xa. Causes less inactivation of thrombin, inhibition of platelets, and bleedingthan standard heparin. Does not significantlyinfluence bleeding time, PT, aPTT. Therapeutic Effect Produces anticoagulation. [Pg.1220]

Micromedex, lepirudin directly inhibits all actions of thrombin. It inhibits free and clot-bound thrombin without requiring endogenous cofactors. Lepirudin is not inhibited by platelet factor 4 and acts independently of antithrombin III and heparin cofactor II. It has no direct effect on platelet function, except inhibition of thrombin-induced platelet activation. No physiological inhibitor of lepirudin is known. [Pg.152]


See other pages where Heparin platelet effects is mentioned: [Pg.148]    [Pg.317]    [Pg.133]    [Pg.258]    [Pg.573]    [Pg.166]    [Pg.269]    [Pg.168]    [Pg.166]    [Pg.146]    [Pg.604]    [Pg.136]    [Pg.149]    [Pg.118]    [Pg.131]    [Pg.133]    [Pg.147]    [Pg.521]    [Pg.298]    [Pg.81]    [Pg.317]    [Pg.319]    [Pg.159]    [Pg.287]    [Pg.116]    [Pg.137]    [Pg.371]    [Pg.589]    [Pg.260]    [Pg.264]    [Pg.399]    [Pg.220]    [Pg.40]    [Pg.256]    [Pg.259]   
See also in sourсe #XX -- [ Pg.143 ]




SEARCH



Heparins platelet

© 2024 chempedia.info