Transient interruption of arterial thrombosis by inhibition of factor Xa results in long-term antithrombotic effects in baboons - PubMed This site needs JavaScript to work properly. Please enable it to take advantage of the complete set of features! Clipboard, Search History, and several other advanced features are temporarily unavailable. Skip to main page content An official website of the United States government Here's how you know The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site. The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. 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Transient interruption of arterial thrombosis by inhibition of factor Xa results in long-term antithrombotic effects in baboons H F Kotzé  1 , S Lamprecht, P N Badenhorst, J P Roodt, V van Wyk Affiliations Expand Affiliation 1 Department of Haematology, University of The Free State, Bloemfontein, Republic of South Africa. GNHMHK@MED.UOVS.AC.ZA PMID: 9241746 Item in Clipboard Transient interruption of arterial thrombosis by inhibition of factor Xa results in long-term antithrombotic effects in baboons H F Kotzé et al. Thromb Haemost. 1997 Jun. Show details Display options Display options Format Abstract PubMed PMID Thromb Haemost Actions Search in PubMed Search in NLM Catalog Add to Search . 1997 Jun;77(6):1137-42. Authors H F Kotzé  1 , S Lamprecht, P N Badenhorst, J P Roodt, V van Wyk Affiliation 1 Department of Haematology, University of The Free State, Bloemfontein, Republic of South Africa. GNHMHK@MED.UOVS.AC.ZA PMID: 9241746 Item in Clipboard Cite Display options Display options Format AbstractPubMedPMID Abstract Recombinant tick anticoagulant peptide (r-TAP) is a potent and specific inhibitor of activated coagulation factor X which effectively interrupts in vivo arterial thrombosis during treatment. It is, however, uncertain if it also affects thrombosis after treatment is stopped. This was tested in a baboon model of arterial thrombosis where platelet deposition onto Dacron vascular graft segments, inserted as extensions into permanent femoral arteriovenous shunts, was measured. The baboons were intravenously treated with 10 micrograms/kg/min (low dose, aPTT = 39 +/- 1 s) and 25 micrograms/kg/min (high dose, aPTT = 58 +/- 2 s) r-TAP for two hours. During treatment the r-TAP inhibited thrombin formation and dose-dependently interrupted platelet deposition onto the graft segment. This effect lasted for up to two hours after treatment with the low dose. Following treatment with the high dose, the graft segments were kept in place for 53 h. After treatment was stopped, platelets again deposited, but at a much lower rate than in control studies. Maximum deposition was approximately 38% lower than in the control studies. Total platelet deposition over 55 h, calculated as the area under the deposition curve, was approximately 40% (p < 0.05) less than in the control studies. A significant shortening in the mean platelet life span and an approximately 15-fold increase in thrombin-antithrombin III complexes during the first 31 h indicated that the thrombus surface remained thrombogenic and that the effect of r-TAP was transient. We have shown that 2 h of treatment with a full antithrombotic dose of r-TAP markedly reduced both the rate of platelet deposition after treatment was stopped and the total number of platelets deposited over 55 h. This was in spite of the finding that the antithrombotic effect of r-TAP was transient. 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