The Antiheparin Effect of α&lt;sub&gt;1&lt;/sub&gt;-Acid Glycoprotein, Evaluated by the Activated Partial Thromboplastin Time and by a Factor Xa Assay for Heparin

Andersen, Per Kragh

doi:10.1159/000214369

Cited by 4 publications

(7 citation statements)

References 2 publications

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“…There have been numerous reports of an anti-heparin activity for AAG, as well as the ability to inhibit platelet aggregation [5][6][7][8][9][10]. In the present study we attempted to simulta neously evaluate the anti-heparin and plate let inhibitory properties ascribed to AAG in PRP.…”

Section: Discussionmentioning

confidence: 95%

“…APTT and HTCT assays in platelet-poor plasma (PPP) confirmed that AAG exhibits a demonstrable anti-heparin effect in these systems [10]. Since AAG also inhibits thrombin-induced activation of isolated platelets [6,7], we combined these reactivi ties and simultaneously monitored platelet aggregation and clot formation stimulated by thrombin or Activated Thrombofax Reagent in the presence and absence of heparin or AAG.…”

Section: Effects O F Aag and Heparin On Platelet Aggregation/clot Formentioning

confidence: 91%

“…Previous investigations revealed AAG to be a potent inhibitor of platelet activation [5][6][7] while additionally serving as a pro-coagu lant by virtue of its reported anti-heparin effects in both activated partial thromboplas tin time (APTT) and heparin thrombin clot ting time (HTCT) assays [8][9][10], As the plate let aggregation and coagulation assays were performed separately in those studies, we felt it important to assess the biological effect(s) of AAG during the coincident generation of each the platelet aggregation and coagulant reactivities. The experiments reported herein illustrate that the anti-heparin effects of AAG in platelet-rich plasma (PRP) are dependent upon which portion of the coagulation cas cade is being initiated as well as concentra tion of heparin employed.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Heparin and α<sub>1</sub>-Acid Glycoprotein on Thrombin or Activated Thrombofax Reagent-Induced Platelet Aggregation and Clot Formation

Fiedel¹,

Costello²,

Gewürz³

et al. 1983

Pathophysiol Haemos Thromb

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α₁-Acid glycoprotein (AAG) obtained from ascites and/or pleural fluids exhibited anti-heparin effects in platelet-poor plasma when evaluated by activated partial thromboplastin (Activated Thrombofax Reagent) and heparin-thrombin clotting time assays. An anti-heparin effect for AAG was also demonstrable in platelet-rich plasma (PRP) challenged with thrombin, but only over a limited range of heparin concentrations; at elevated heparin concentrations, and only in the presence of AAG, both platelet aggregation and clot formation were substantially inhibited. However, no detectable anti-heparin effect was observed following challenge of PRP with Activated Thrombofax Reagent; indeed, the anti-coagulant effect of heparin appeared synergistically amplified in these systems containing AAG, and AAG exhibited platelet pro-aggregate and pro-coagulant properties in the absence of heparin. The platelet pro-aggregating activity of AAG, though independent of heparin, appeared to require the onset of the coagulation cascade prior to the generation of thrombin; in the absence of such initiation, AAG remained a potent inhibitor of platelet activation.

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Section: Discussionmentioning

confidence: 95%

Section: Effects O F Aag and Heparin On Platelet Aggregation/clot Formentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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Effects of Heparin and α<sub>1</sub>-Acid Glycoprotein on Thrombin or Activated Thrombofax Reagent-Induced Platelet Aggregation and Clot Formation

Fiedel¹,

Costello²,

Gewürz³

et al. 1983

Pathophysiol Haemos Thromb

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“… 101 Alpha-1-acid glycoprotein can neutralize heparin but only when present at high concentrations, such as those that occur during inflammation. 67 , 68 An injection of heparin could potentially saturate the transport site on the protein and prevent it from carrying other drugs or molecules.…”

Section: Gag Neutralization During Inflammationmentioning

confidence: 99%

Glycosaminoglycan Neutralization in Coagulation Control

Sobczak

Pitt

Stewart

2018

ATVB

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The glycosaminoglycans (GAGs) heparan sulfate, dermatan sulfate, and heparin are important anticoagulants that inhibit clot formation through interactions with antithrombin and heparin cofactor II. Unfractionated heparin, low-molecular-weight heparin, and heparin-derived drugs are often the main treatments used clinically to handle coagulatory disorders. A wide range of proteins have been reported to bind and neutralize these GAGs to promote clot formation. Such neutralizing proteins are involved in a variety of other physiological processes, including inflammation, transport, and signaling. It is clear that these interactions are important for the control of normal coagulation and influence the efficacy of heparin and heparin-based therapeutics. In addition to neutralization, the anticoagulant activities of GAGs may also be regulated through reduced synthesis or by degradation. In this review, we describe GAG neutralization, the proteins involved, and the molecular processes that contribute to the regulation of anticoagulant GAG activity.

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“…This variation, also known as the heparin neutralizing activity, may be due to individual variations in platelet factor 4 availability and also differences in concentration of various plasma proteins, i.e. al-acid glycoprotein (Godal 1961, Andersen 1980).…”

Section: Discussionmentioning

confidence: 99%

Heparin Levels and Activated Clotting Time (ACT) during Open Heart Surgery

Stenbjerg

Berg

Albrechtsen

1981

Scandinavian Journal of Haematology

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Heparin levels were followed by an amidolytic method during open heart surgery in 10 adult patients and correlated to the activated clotting time (ACT) (Haemochron®). There was a good correlation between the 2 parameters when the ACT was below 600 s. Based on the present and previous studies of the ACT the authors conclude that the ACT is a useful tool in control of heparinization during open heart surgery.

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The Antiheparin Effect of α<sub>1</sub>-Acid Glycoprotein, Evaluated by the Activated Partial Thromboplastin Time and by a Factor Xa Assay for Heparin

Cited by 4 publications

References 2 publications

Effects of Heparin and α<sub>1</sub>-Acid Glycoprotein on Thrombin or Activated Thrombofax Reagent-Induced Platelet Aggregation and Clot Formation

Effects of Heparin and α<sub>1</sub>-Acid Glycoprotein on Thrombin or Activated Thrombofax Reagent-Induced Platelet Aggregation and Clot Formation

Glycosaminoglycan Neutralization in Coagulation Control

Heparin Levels and Activated Clotting Time (ACT) during Open Heart Surgery

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