title: In vitro platelets/endothelial cells interactions in presence of acetylsalicylic acid at various dosages.
abstract: Venous endothelium is able to release in vitro substances which modifies platelet aggregation. A vascular fragment incubated in Michaelis buffer (pH 7.30), aliquoted and tested on platelet-rich-plasma partially inhibits the aggregometry parameters. Addition of acetylsalicylic acid (ASA) at ultra low dose (0.1 nM final solution in the incubation tube) presents a reversed effect on this inhibition. To explain this phenomenon, 6-keto-PGF1 alpha and von Willebrand factor were dosed in the incubation media. After determination of an active level of 6-keto-PGF1 alpha (200 pg/100 microliters), 2 series were made: series 1 included the values below 200 pg/100 microliters incubation media, series 2, the values above 200 pg/100 microliters incubation media. When the vascular fragment was incubated as described above, the results of aggregometry ratio for series 1 were: test A (without ASA): 0.84 +/- 0.18, test B1 (with 0.1 nM of ASA): 0.87 +/- 0.13. For series 2, they became: test A: 0.75 +/- 0.27, test B1: 0.93 +/- 0.16. Control was always: 1.00 +/- 0.00. For the same groups, 6-keto-PGF1 alpha values were: for series 1, test A: 81 +/- 57, test B1: 81 +/- 60 pg/100 microliters incubation medium, for series 2, test A: 596 +/- 495, test B1: 383 +/- 263 pg/100 microliters incubation medium. Analyses were also performed with 2 high doses of ASA (B2: 10(5) nM and B3: 10(6) nM final solution) in the same experimental conditions. In these groups, aggregation parameters were decreased (0.86 +/- 0.14 for 10(5) nM, 0.84 +/- 0.15 for 10(6) nM) as well as 6-keto-PGF1 alpha production (189 +/- 199 for 10(5) nM, 152 +/- 182 for 10(6) nM). For these two last ASA treatments, comparison of the results in groups set up according to the sensitive 6-keto-PGF1 alpha value (200 pg/100 microliters solution) showed no modification. So it seems that a certain reactive state, specific of ultra low dose treatment is necessary for the vascular endothelium to be sensitive at such treatment.
authors.affiliation: Laboratoire d'Hématologie, Bordeaux, France.
authors.forename: M C
authors.initials: MC
authors.lastname: Lalanne
authors.forename: I
authors.initials: I
authors.lastname: Ramboer
authors.forename: O
authors.initials: O
authors.lastname: de Sèze
authors.forename: C
authors.initials: C
authors.lastname: Doutremepuich
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D001241:Aspirin / Q000008:administration & dosage* / Q000494:pharmacology; D001792:Blood Platelets / Q000166:cytology / Q000187:drug effects*; D002450:Cell Communication / Q000502:physiology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects*; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D011863:Radioimmunoassay; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D010975:Platelet Aggregation Inhibitors; D014841:von Willebrand Factor; D015121:6-Ketoprostaglandin F1 alpha; D001241:Aspirin