Pharmacologic effects of nicotinic acid on human purine metabolism.
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Adult↗
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Results for “SULFINPYRAZONE”
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Bradykinin induced bronchoconstriction in guinea pigs and its modification by various agents.
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Analgesics↗
Status of antiplatelet drugs in coronary heart disease.
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Aspirin↗
[Cutaneous side effects of systemic drugs with special reference to recently introduced medicaments. I].
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Allopurinol↗
Management of thrombotic diseases.
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Anticoagulants↗
[Incidence of thrombosis and the status of coagulation in ischaemic heart disease].
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Acute Disease↗
Effect of antilymphocyte globulin on platelets.
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Antilymphocyte Serum↗
Rapidly progressive glomerulonephritis treated with anticoagulants.
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Adult↗
[Current status of vascular diseases and their treatment].
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Arteriosclerosis↗
Effect of drugs that suppress platelet surface interaction on incidence of amaurosis fugax and transient cerebral ishcemia.
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Blindness↗
The prevention of thrombosis.
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Anti-Inflammatory Agents↗
Effect of Newcastle disease virus on human or rabbit platelets. Aggregation and loss of constituents.
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Adenine Nucleotides↗
[Medical therapy of thrombosis].
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Anticoagulants↗
Recognizing and reacting to recurrent pulmonary embolism.
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Administration, Oral↗
Activation of the Hageman factor-prekallikrein system in the pathogenesis of the generalized Shwartzman reaction and of the hepatic vein thrombosis phenomenon in the rat.
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Animals↗
Heterophile antibodies and tissue injury. 3. A role for platelets in the development of lethal vascular injury during Forssman shock in guinea pigs.
Platelets appear to be pathogenetic determinants in the development of lethal Forssman shock, which was provoked in guinea pigs by an intravenous injection of rabbit antiserum to sheep erythrocyte stromata. Within moments, circulating platelets (prelabeled with (14)C-serotonin) were removed from the blood stream and impacted in the lungs, where they liberated (14)C into the tissues. When animals were depleted of platelets prior to the production of shock, they survived for prolonged periods of time or were protected against death. Pretreatment with antiinflammatory compounds capable of inhibiting platelet aggregation and release phenomena had a similar protective influence. It would appear, therefore, that Forssman shock is a convenient and accessible model for investigating the mechanisms whereby platelets mediate immune vascular damage.
Anaphylaxis↗