Conventional heparin and semisynthetic heparin analogue (SSHA) alteration of blood coagulation after embolic occlusion of human renal circulation
Autor: | L. E. Almgård, Margareta Blombäck, Nyman Cr, Törngren S, U. Norming |
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Rok vydání: | 1990 |
Předmět: |
Male
medicine.medical_specialty medicine.drug_class medicine.medical_treatment Renal Circulation chemistry.chemical_compound Internal medicine Fibrinolysis Humans Medicine Blood Coagulation Carcinoma Renal Cell Aged Renal circulation Factor VII Heparin business.industry Chondroitin Sulfates Antithrombin Anticoagulant Anticoagulants Hematology Middle Aged Embolization Therapeutic Kidney Neoplasms Endocrinology medicine.anatomical_structure Coagulation chemistry Anesthesia Female business medicine.drug Blood sampling |
Zdroj: | Thrombosis Research. 59:237-246 |
ISSN: | 0049-3848 |
DOI: | 10.1016/0049-3848(90)90127-x |
Popis: | Blood coagulation and fibrinolytic variables were measured in a peripheral vein in a studv f 21 consecutive patients before and after angio-embolization of renal carcinoma. The first ten patients received conventional heparin, 5000 IU twice daily, and the following eleven a semi-synthetic heparin analogue (SSHA), 50 mg twice daily, for 5 days. The first injection was given 2 hours before embolization and the last injection at least 12 hours before the last blood sampling. Both groups showed increased levels of FPA on day 5–7, indicating that the anticoagulant influence had ceased. F VII levels decreased only in the SSHA group from embolization to day 3, but were increased in both groups on day 5–7. Levels of thrombin-antithrombin complexes (TAT) were significantly increased in the heparin group 2 hours after embolization, indicating that thrombin activity had been formed. The corresponding TAT level in the SSHA group was not significantly increased. The differences could possibly indicate a different mechanism of action on blood coagulation of SSHA as compared with heparin, with involvement of extrinsic pathway and maybe by-passing antithrombin III inhibition. |
Databáze: | OpenAIRE |
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