2007
DOI: 10.1016/j.hoc.2006.11.012
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Platelet Inhibitors and Monitoring Platelet Function: Implications for Bleeding

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Cited by 6 publications
(4 citation statements)
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“…These results are in line with previous reports, where the use of nonselective NSAIDs (ketoprofen), in spite of decreasing platelet aggregation, did not increase BMBT in dogs undergoing surgery . The lack of a substantial impact of decreased platelet function on viscoelastic properties of the fibrin clot assessed by thromboelastometry or thromboelastography has also been reported in the literature . These results must be carefully interpreted as the effects of these drugs were not evaluated in animals with hemostatic disturbances (hemorrhage or thrombosis) or those at risk for developing such conditions.…”
Section: Discussionsupporting
confidence: 91%
See 1 more Smart Citation
“…These results are in line with previous reports, where the use of nonselective NSAIDs (ketoprofen), in spite of decreasing platelet aggregation, did not increase BMBT in dogs undergoing surgery . The lack of a substantial impact of decreased platelet function on viscoelastic properties of the fibrin clot assessed by thromboelastometry or thromboelastography has also been reported in the literature . These results must be carefully interpreted as the effects of these drugs were not evaluated in animals with hemostatic disturbances (hemorrhage or thrombosis) or those at risk for developing such conditions.…”
Section: Discussionsupporting
confidence: 91%
“…Although dipyrone alone or combined with meloxicam significantly inhibited platelet aggregation in the study reported here, the viscoelastic properties of clot formation were unaltered by these drugs. These results were expected because the 2 techniques currently available for evaluating the viscoelastic properties of clot formation and dissolution over time (ROTEM and thromboelastography) are insensitive to evaluate the antiplatelet effects of aspirin . This limitation occurs largely because thrombin formation during the conventional ROTEM and the thromboelastography procedure leads to significant platelet activation via thrombin formation that masks any in vivo platelet inhibition by less potent platelet activators.…”
Section: Discussionmentioning
confidence: 99%
“…The final common pathway of platelet aggregation leading to coronary thrombosis involves cross-linking of platelet receptor glycoprotein (GP) IIb-IIIa by adhesive plasma proteins, primarily fibrinogen. 35 Abciximab, eptifibatide, and tirofiban block this final common pathway and are considered the most powerful platelet inhibitors. Time to normal platelet aggregation is 24 to 48 hours after administration of abciximab, and eptifibatide and tirofiban require 4 to 8 hours.…”
Section: Glycoprotein Iib-iiia Receptor Antagonistsmentioning
confidence: 99%
“…O sangue humano apresenta normalmente de 200.000 a 400.000 plaquetas/mm 3 . 10,11 Em condições normais, as plaquetas circulam no sangue em estado de repouso sob a forma discóide, sendo impedidas de interagir com a matriz subendotelial graças ao endotélio vascular que funciona como uma barreira que exerce ativamente funções antiadesivas e antiagregantes, principalmente através da liberação de PGI 2 e óxido nítrico (NO). Entretanto, quando recrutadas devido a alterações dessas células endoteliais e à exposição de moléculas do subendotélio, principalmente colágeno e fator de von Willebrand, as plaquetas sofrem uma drástica mudança morfológica.…”
Section: Hemostasia Primáriaunclassified