931-111 Platelet Activation and Aggregation by Therapeutic Doses of Heparin
نویسندگان
چکیده
منابع مشابه
Effect of heparin and heparin fractions on platelet aggregation.
Porcine intestinal mucosal heparin induced aggregation of platelets in citrated platelet-rich plasma and enhanced platelet aggregation and serotonin secretion induced by other agents. This action of heparin was blocked by substances that elevate platelet cyclic AMP and by EDTA but not by inhibitors of platelet cyclooxygenase. The effect was not inhibited by apyrase or by N-amylthio-5'-AMP and t...
متن کاملEffect of Heparin and Heparin Fractions on Platelet Aggregation
cofactor required for ristocetin. Fractionation of heparin yielded preparations that varied in molecular weight and, within a given molecular weight fraction, in affinity for antithrombin III. Fractions of high molecular weight (average 20,000) were more reactive with platelets than were fractions of low molecular weight (7,000). Anticoagulant activity did not parallel the platelet reactivity o...
متن کاملDirect detection of heparin-induced platelet aggregation.
Platelet Aggregation To the Editor: Enhanced platelet aggregation responses to stimulation with ADP or thrombin receptor agonist peptides (TRAP) have been observed during heparin therapy in patients with unstable angina. However, the platelet aggregation curve in Figure 3 of the article by Xiao and Théroux1 was not obtained from a direct detection to evaluate heparin-induced hyperaggregation. A...
متن کاملChylomicron-induced prothrombin activation and platelet aggregation.
The effects on platelet aggregation of native rat chyle chylomicrons, chylomicron remnants, and chylomicrons that had been preincubated with rat or human EDTA-plasma, serum, whole blood, or pure human prothrombin were examined. The native chyle chylomicrons did not induce platelet aggregation but decreased ADP- and thrombin-induced platelet aggregation and [14C]serotonin release. Chylomicron re...
متن کاملof platelet aggregation . Fibrinogen mediated activation
diagnosed by morphological, cytochemical, immunological, and ultrastructural methods.' Following remission induction with daunorubicin, vincristine, prednisolone, and L-asparaginase she received maintenance treatment with methotrexate, 6 mercaptopurine, cytosine arabinoside, vincristine, and prednisolone for 12 months before this was stopped due to neutropenia. She remained well until August 19...
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ژورنال
عنوان ژورنال: Journal of the American College of Cardiology
سال: 1995
ISSN: 0735-1097
DOI: 10.1016/0735-1097(95)91939-u