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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0005729,
umls-concept:C0005821,
umls-concept:C0030956,
umls-concept:C0182437,
umls-concept:C0243144,
umls-concept:C0250908,
umls-concept:C0330390,
umls-concept:C0597357,
umls-concept:C0750502,
umls-concept:C0947693,
umls-concept:C1280500,
umls-concept:C1292733,
umls-concept:C1706968,
umls-concept:C2003941
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pubmed:issue |
4
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pubmed:dateCreated |
1994-11-7
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pubmed:abstractText |
Synthetic vascular prostheses lack the uniquely low thrombogenicity provided by the endothelial cell lining of autogenous saphenous vein or artery grafts. The thrombogenic nature of the synthetic graft surface becomes a major determinant of early prosthetic graft patency. We demonstrate in a baboon ex vivo synthetic graft model that modification of the host's platelet interaction with the graft surface results in inhibition of platelet thrombus formation and thereby, a possible enhancement of early prosthetic graft patency. This was achieved by selective blockage of the platelet alpha IIb beta 3 receptor by the arginine-glycine-aspartic acid-containing synthetic peptide TP9201. Platelet thrombus formation on a Dacron graft indicated by accumulation of indium III-oxine-labeled autologous platelets was measured by gamma camera imaging. After 60 minutes of circulation, TP9201 at a bolus of 125 micrograms/kg; infusion of 3 micrograms/kg/min, bolus of 190 micrograms/kg; infusion of 5 micrograms/kg/min, bolus of 250 micrograms/kg; infusion of 6 micrograms/kg/min, and bolus of 500 micrograms/kg; infusion of 12 micrograms/kg/min decreased platelet uptake on the graft to 50%, 40%, 30%, and 10% of control uptake, respectively. Forelimb template bleeding times were not found to be significantly prolonged at doses that effectively inhibit ex vivo platelet aggregation. As a result of drug treatment, no changes in hemodynamic parameters or hematologic profile, including platelet number and clotting time, were observed. We demonstrate here that the arginine-glycine-aspartic acid-containing peptide TP9201, which competitively inhibits the alpha IIb beta 3 integrin-fibrinogen interaction, significantly decreased the accumulation of platelets on a Dacron vascular graft. Molecules like peptide TP9201, because of its unique activity profile, may represent a superior approach to the control of platelet accumulation on thrombogenic surfaces.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Integrins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides, Cyclic,
http://linkedlifedata.com/resource/pubmed/chemical/Platelet Aggregation Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Platelet Glycoprotein GPIIb-IIIa...,
http://linkedlifedata.com/resource/pubmed/chemical/Polyethylene Terephthalates,
http://linkedlifedata.com/resource/pubmed/chemical/TP 9201
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-2143
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
124
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
589-99
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:7523555-Animals,
pubmed-meshheading:7523555-Bleeding Time,
pubmed-meshheading:7523555-Blood Platelets,
pubmed-meshheading:7523555-Blood Vessel Prosthesis,
pubmed-meshheading:7523555-Dose-Response Relationship, Drug,
pubmed-meshheading:7523555-Hemodynamics,
pubmed-meshheading:7523555-Integrins,
pubmed-meshheading:7523555-Male,
pubmed-meshheading:7523555-Papio,
pubmed-meshheading:7523555-Peptides, Cyclic,
pubmed-meshheading:7523555-Platelet Aggregation Inhibitors,
pubmed-meshheading:7523555-Platelet Glycoprotein GPIIb-IIIa Complex,
pubmed-meshheading:7523555-Polyethylene Terephthalates,
pubmed-meshheading:7523555-Vascular Patency
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pubmed:year |
1994
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pubmed:articleTitle |
Selective alpha IIb beta 3 receptor blockage with peptide TP9201 prevents platelet uptake on Dacron vascular grafts without significant effect on bleeding time.
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pubmed:affiliation |
Surgical Research Laboratory, New England Medical Center, Boston.
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pubmed:publicationType |
Journal Article
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