A model for ultrasound absorption and dispersion in dilute suspensions of nanometric contrast agents

2012 ◽  
Vol 132 (6) ◽  
pp. 3748-3759 ◽  
Author(s):  
François Coulouvrat ◽  
Jean-Louis Thomas ◽  
Ksenia Astafyeva ◽  
Nicolas Taulier ◽  
Jean-Marc Conoir ◽  
...  
1998 ◽  
Vol 80 (08) ◽  
pp. 266-272 ◽  
Author(s):  
Andrew Parker ◽  
William Fay

SummaryClinical trials suggest that the risk of thrombosis during coronary angioplasty is lower with ionic contrast agents than with nonionic contrast agents. However, the molecular mechanisms underlying this effect are unknown. This study examined the effects of contrast agents on thrombin formation and its interaction with substrates, inhibitors, and ligands to define potential mechanisms by which contrast agents affect thrombus formation. Two ionic agents, diatrizoate and ioxaglate, and one nonionic agent, ioversol, were studied. Ionic agents inhibited factor X activation by the tissue factor-factor VIIa complex more potently than ioversol (53 ± 3.7, 43.0 ± 1.9, and 26.5 ± 2.4% inhibition by diatrizoate, ioxaglate, and ioversol, respectively, at concentrations of 5%). Ionic contrast agents were potent inhibitors of prothrombinase function, inhibiting thrombin formation by >75% at contrast concentrations of 0.6% (p <0.005). Ioversol inhibited prothrombinase to a significantly lesser extent than ionic agents. Clotting assays suggested that ioxaglate was the most potent inhibitor of thrombin generation in plasma despite having the least effect on fibrin polymerization. Contrast agents inhibited binding of thrombin to fibrin, with ionic agents producing a more potent effect than ioversol (p <0.02). However, contrast agents did not inhibit thrombin-mediated platelet activation, had only a minor effect on inhibition of thrombin by antithrombin III, and did not affect thrombin-hirudin interactions. In summary, these studies identify specific mechanisms by which radiographic contrast agents inhibit thrombin formation and function – i.e. inhibition of tissue factor-dependent factor Xa generation, inhibition of the prothrombinase complex, and inhibition of thrombin binding to fibrin. These findings may help to explain the reduced risk of thrombosis during coronary angioplasty associated with ionic contrast agents.


1977 ◽  
Vol 38 (02) ◽  
pp. 0420-0428 ◽  
Author(s):  
J. L Moake ◽  
P. L Cimo ◽  
K Widmer ◽  
D. M Peterson ◽  
J. R Gum

SummaryIn dilute suspensions of platelet-rich plasma (PRP) or gel-separated platelets (GSP), dibutyryl-cAMP (DBcAMP) and monobutyryl-cAMP inhibited platelet-mediated fibrin clot retraction in concentrations of 2–3 × 10–6M, with complete inhibition at 1–3 × 10–4M. Prostaglandin E1 (PGE1), which inhibited fibrin clot retraction in concentrations greater than 1.5–3 × 10–8M, was a more effective inhibitor than either PGE2 or PGF2α. In the presence of theophylline (10–4M), concentrations of DBcAMP, PGE1 PGE2 and PGF2α necessary to inhibit fibrin clot retraction were reduced 50-fold for DBcAMP and 2.5 to 20-fold for the prostaglandins. In dilute PRP or GSP, inhibition of fibrin clot retraction does not result from inhibition of thrombin-induced platelet aggregation. Thus, compounds which increase platelet cAMP levels result in the inhibition of platelet-mediated fibrin clot retraction, and this inhibitory effect may be mediated, at least in part, through suppression of platelet contractility. Cyclic GMP, dibutyryl-cGMP and carbamylcholine-Cl (which stimulates guanylate cyclase) did not influence fibrin clot retraction, and did not prevent inhibition of fibrin clot retraction by DBcAMP and PGE?. Colchicine, in concentrations known to disrupt platelet microtubules (2.5 × 10–6M to 2.5 x 10–3M), had little inhibitory effect on either fibrin clot retraction or platelet (3H)-serotonin release.


2014 ◽  
Vol 59 (1) ◽  
pp. 50-57 ◽  
Author(s):  
I.O. Lysiuk ◽  
◽  
Ya.M. Olikh ◽  
O.Ya. Olikh ◽  
G.V. Beketov ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document