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Biomedical subjects

F Potevin

Publications and source records attributed to F Potevin.

10 recordsLinked to original sources
PubMed1992

Acquired von Willebrand disease: correction of hemostatic defect by high-dose intravenous immunoglobulins.

High-dose intravenous immunoglobulins (ivIG) were used in a 57-year-old patient with acquired von Willebrand disease in order to correct a hemostatic defect before pneumonectomy for lung carcinoma. IvIG induced a rapid and complete correction of factor VIII (F VIII) and von Willebrand factor (vWF) and allowed surgery without additional factor coverage. F VIII and vWF returned to baseline values within 10 days after ivIG.

Dose-Response Relationship, Drug↗
PubMed1991

Rapid aequorin loading into platelets in the presence of DMSO--characteristics of the responses (changes in light transmission and in calcium) to various agonists.

We have looked at different parameters which could modify platelet behaviour during and after aequorin loading in the presence of DMSO. There is a decreased platelet reactivity in response to ADP, PAF and A-23,187 which appears to be mainly due to the exposure to EGTA during washing and loading and the 1 ml volume of the test suspension. All the studied agonists (including PMA) which elicit aggregation are able to induce an intracellular Ca2+ change detected with the aequorin probe. By contrast, epinephrine alone induces neither aggregation nor Ca2+ rise, but potentiates the responses to ADP. Different consecutive phases in Ca2+ changes after stimulation with ADP, PMA and A-23,187 can be evidenced. In the presence of external Ca2+, the second component of the Ca2+ change evoked with ADP is dependent on aggregation and the subsequent TXA2 synthesis. When the external medium is Ca2+ depleted, the two Ca2+ peaks induced by ADP disappear whereas a Ca2+ rise persists (endogenous mobilization) with the other agonists, being independent of TXA2 and ADP release. Ca2+ mobilization parallels activation with A-23,187 but not with low concentrations of thrombin.

Aequorin↗
PubMed1990

Aequorin-detected calcium changes in stimulated thrombasthenic platelets. Aggregation-dependent calcium movement in response to ADP.

Calcium changes in normal and thrombasthenic platelets were recorded using the PICA-apparatus. Aequorin was loaded in the presence of DMSO, EGTA and PGE1. Platelets of three patients with type I thrombasthenia stimulated with A-23, 187, thrombin, PMA in the presence 1 mM Ca++ and 1 mM Mg++ were able to normally raise their calcium concentrations. The maximal values could be found below the normal range with collagen, ADP and PAF-acether. Calcium mobilization from internal stores in response to thrombin was normal. There were two calcium peaks in normal platelets stimulated with ADP. The second one was suppressed by omitting fibrinogen, stirring, or by adding aspirin, and was absent in thrombasthenic platelets. Thus the GP IIb-IIIa complex is not a prerequisite for calcium fluxes but is involved, when weak agonists such ADP are used, through an aggregation-dependent reinforcement of platelet activation.

Adenosine Diphosphate↗
PubMed1990

Inhibition of platelet activation by the nitrate Sin-1: studies with human aequorin-loaded platelets.

The effects of the nitrovasodilator Sin-1, which is thought to work through cyclic-GMP, were studied using human, aequorin-loaded, washed platelets. Changes in light transmission (shape change, aggregation), and in intracellular calcium were simultaneously recorded. Evidence was obtained for an inhibitory effect distal to calcium changes, in a similar way than a prostacyclin analogue, Iloprost. By contrast the response to an activator of protein kinase C was unaffected. There was a partial, parallel decrease in calcium changes and aggregation induced with thrombin, and a total inhibition of the responses to ADP (linked to a calcium influx).

Aequorin↗
PubMed1989

Calcium rise in human platelets elicited by anti-CD9 and -CD41 murine monoclonal antibodies.

Three murine monoclonal antibodies (anti-CD9: ALB6, anti-CD41: VI-PL3 and PL2-49/GPIIb - final concentration: 7.5 micrograms/mL) are shown to elicit after a lag time aggregation of washed platelets and a calcium signal (as detected by light emitted by loaded aequorin), which is only partially inhibited by aspirin. By comparison the rise induced by thrombin is greater and almost instantaneous. In the presence of EGTA a calcium mobilization from internal stores can be detected with thrombin and with ALB6, but neither with PL2-49 nor with VI-PL3, whereas platelets still change their shape and release ATP. It is tempting to speculate that although all the antibodies induce a calcium change, they activate platelets by different pathways: calcium may be not primarily involved in the activation induced by the anti-CD41 antibodies.

Adenosine Triphosphate↗
PubMed1989

PL2-49, a monoclonal antibody against glycoprotein IIb which is a platelet activator.

PL2-49 is a murine monoclonal IgG1 antibody obtained after immunization of Balb/c mice with EDTA washed platelets. Binding could be detected on Zwa(+) as well as Zwa(-) platelets, but not on type I Glanzmann's thrombasthenia platelets using an ELISA screening test. Immunoprecipitation studies showed that PL2-49 bound to glycoprotein IIb when the glycoprotein IIb/IIIa complex dissociation was performed after the monoclonal antibody binding. Experiments with a human alloantibody against Zwa antigen were run in parallel to control the complex dissociation. Ascitic fluid, as well as the purified antibody, induced activation and aggregation of washed platelets and ATP release. PL2-49-induced aggregation did not require exogenous fibrinogen and was inhibited, partially, in the presence of aspirin, apyrase, isosorbide dinitrate. Raising intra-platelet cyclic AMP with a stable PGI2 analogue, iloprost, and/or a phosphodiesterase inhibitor, RA 233, suppressed the responses to PL2-49. F(ab')2 fragments did not induce aggregation of normal platelets but inhibited the response to the whole immunoglobulin. Finally PL2-49 was shown to induce aequorin-detected elevations in intraplatelet Ca++ levels. Thus PL2-49 seems to differ from monoclonal antibodies so far described, since it binds to glycoprotein IIb in a complex-dependent manner at least under our experimental conditions for immunoprecipitation studies, and it induces platelet Ca++ mobilization and platelet aggregation after a lag-time. These reactions depend both on Fab and Fc domains of the antibody and require neither complement nor exogenous fibrinogen.

Animals↗
PubMed1987

[Platelet aggregation tests in 26 cases of heparin-induced thrombopenia. Methodological, diagnostic problems and therapeutic aspects].

A diagnosis of heparin induced thrombocytopenia (HIT) in the 26 patients was based on: 1. normal platelet count prior to heparin administration; 2. its fall to less than 100 Giga/l (m = 46 +/- 23) at time of first sample collection for test to detect a platelet aggregation factor (PAF); 3. restoration of normal values after discontinuation of heparin treatment during which the thrombocytopenia had appeared. The result of the first PAF test in these 26 patients was positive in 22 cases, negative in 2; twice the plasma provoked platelet control aggregation without in vitro addition of heparin. The origin, dose and mode of administration of the heparin did not appear determinant in the production of the thrombocytopenia: 16 of the patients were later treated with a low molecular weight heparin (LMWH). An in vitro "compatibility" test was able to be performed 8 times previously and was negative in 7 cases in the 16 patients. Samples were collected during LMWH treatment and were negative in 13 cases, and this in agreement with the increased platelet count after 7 +/- 3 days and the clinical improvement. In 3 patients the test was positive: in one case the count did not return to normal, in the second case this did occur, but slowly (21 days); the PAF test in the last patient was positive prior to LMWH treatment and remained so while the count became normal. Concordance exists therefore between negativity of the test practiced with LMWH and the increase in count when this heparin is administered; inversely, the positivity of the test does not exclude normalization of the platelet count.

Adult↗