Gender differences in hemorheological parameters and in in vitro platelet aggregation in acetylsalicylic acid and clopidogrel treated vascular patients

Biorheology ◽  
2014 ◽  
Vol 51 (2-3) ◽  
pp. 197-206 ◽  
Author(s):  
Katalin Koltai ◽  
Judit Papp ◽  
Peter Kenyeres ◽  
Gergely Feher ◽  
Antal Tibold ◽  
...  
Keyword(s):  
Gender Differences ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid

Effect Of Factor XIII On Platelet Aggregation. Study Of Platelet Function And Fibrin Stabilization Inhibitors

1981 ◽  
Author(s):  
M Maamer ◽  
O Demay ◽  
M Aurousseau
Keyword(s):  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Platelet Function ◽  
Factor Xiii ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Photometric Method

There is little information on the participation of Factor XIII in platelet aggregation. Using BORN’s photometric method to study platelet aggregation induced by ADP in vitro on platelet rich plasma (PRP) of rabbit; clot solubility in 1 % monochloracetic acid and incorporation of dansylcadaverin into casein (LORAND L. et al.) to measure plasma FXIII concentration ; we showed that addition of activated F.XIII (F.XIIIa) to a PRP, aggregating power of platelets was significantly increased (+ 30.4 %, p<0.00l). Addition of inactive F.XIII or thrombin + Ca++ in concentrations used to activate F.XIII, had no significant effect on platelet aggregation induced by ADP.When F.XIIIa was added to plasma in presence of F.XIII inhibitors as 3178 AQ (a new synthetic benzothiophen keton derivative) or monodansylcadaverin (DC) in concentrations of (3.27 × 10-4 M and 9.31 × 10-4 m respectively), the platelet aggregation was significantly inhibited (- 48.8 % and - 35.4 % respectively, p<0.001). This inhibitory effect was not seen when dipyridamole or Acetylsalicylic Acid (ASA) in concentrations of (6.18 × 10-4 M and 17.3 × 10-4 M respectively) ware added in PRP in presence of F.XIIIa When platelet aggregation was performed without addition of F.XIIIa the inhibitory effect of 3178 AQ and DC was respectively (- 76.6 % and - 65.1 %, p<0.001), dipyridamole (- 37.6 %, p<0.00l) and ASA (-4.1%, no significant)These results suggest that F.XIIIa increased the platelet aggregation induced by ADP and compounds which are both inhibitors of platelet aggregation and F.XIII would be more potent antithrombotic by acting on platelets and fibrin stabilization, than drugs which are inhibitors of platelet aggregation only.

The Antiplatelet Effects of a New Nitroderivative of Acetylsalicylic Acid - An In Vitro Study of Inhibition on the Early Phase of Platelet Activation and on TXA2 Production

1996 ◽  
Vol 76 (05) ◽  
pp. 791-798 ◽  
Author(s):  
Clara Lechi ◽  
Giuseppe Andrioli ◽  
Stefania Gaino ◽  
Rosamaria Tommasoli ◽  
Valeria Zuliani ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Platelet Activation ◽  
Cyclic Gmp ◽  
Thromboxane A2 ◽  
Antiplatelet Activity ◽  
Ncx 4016

SummaryWe studied in vitro the antiplatelet activity of a new nitroderivative chemically related to acetylsalicylic acid: 2 acetoxybenzoate 2-[l-nitroxy-methyl]-phenyl ester (NCX 4016), in order to identify any effects due to the release of nitric oxide and the blockade of cyclooxygenaseThe effects of scalar doses of NCX 4016 on the early phase of platelet activation, platelet aggregation and thromboxane A2 production were investigated. We observed inhibitory effects of NCX 4016 on platelet adhesion (IC50 = 7.3 × 10−5 M), platelet cytosolic calcium concentration, assayed by fluorescent probe Fura 2, and the expression of glycoprotein IMIIa (CD41 / αIIbβ3) (IC50 = 3.4 × 10−5 M) and P-selec-tin (CD62 / GMP-140) (IC50 = 4.9 × 10−5 M) measured by flow cytometry. NCX 4016 also prevented thrombin-induced platelet aggregation (IC50 = 3.9 × 10−5 M). None of these parameters were affected by acetylsalicylic acid. These inhibitory activities of NCX 4016 were abolished by oxyhaemoglobin and methylene blue. Intracellular cyclic GMP observed during thrombin-induced aggregation was increased by incubation with NCX 4016. These results appear to be attributable to the release of nitric oxide, which activates soluble platelet guanylyl-cyclase and promotes intracellular cyclic GMP increase. NCX 4016 almost completely inhibited platelet thromboxane A2 production and arachidonic acid-induced platelet aggregation. This also occurred in the presence of oxyhaemoglobin and methylene blue, indicating that its antiplatelet activity can be attributed not only to nitric oxide release but also to cyclo-oxygenase inhibition.

scholarly journals Effects on thrombocytic hemostasis of a new derivate indolinone

2019 ◽  
Vol 18 (3) ◽  
pp. 574-576
Author(s):  
VV Bykov ◽  
V Yu Serebrov ◽  
VV Udut ◽  
EV Udut ◽  
VP Fisenko
Keyword(s):  
Diabetes Mellitus ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Medical Science ◽  
Antiplatelet Drug ◽  
Control Group ◽  
Antiplatelet Activity ◽  
Wide Range

Objective. Specific activity of an antiplatelet drug of indolinone series (codenamed DI) was studied in vitro in a model of ADP-induced platelet aggregation in vitro and in vivo in a model of streptozotocininduced diabetes mellitus in rats. Material and Methods. Acetylsalicylic acid and dipyridamole were used as reference drugs. In vitro tests have demonstrated that DI exhibits antiplatelet activity in a wide range of concentrations (0,75×10-6 – 1.5×10-5 М, р<0,05), being comparable to acetylsalicylic acid and dipyridamole. In vivo tests have demonstrated dose-dependent antiplatelet activity of DI in doses of 2,5 – 20 mg/kg (21-14 %). Results and Discussion.Increasing the dose of DI above 10 mg/kg doesn’t increase its antiplatelet activity. After multiple oral administration to rats with streptozotocin-induced diabetes mellitus in 10 mg/kg dose, DI has exhibited antiplatelet activity, reducing the platelet aggregation rate to that of the control group (р<0,05). Conclusion. Thus, DI isapromisingcompound for furtherdevelopmentof an antiplatelet drug with new mechanism of action Bangladesh Journal of Medical Science Vol.18(3) 2019 p.574-576

scholarly journals Antiplatelet activity of new derivatives of benzimidazole containing sterically hindered phenolic group in their structure

2020 ◽  
Vol 6 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Alexander A. Spasov ◽  
Aida F. Kucheryavenko ◽  
Ksenia A. Gaidukova ◽  
Vadim A. Kosolapov ◽  
Olga N. Zhukovskaya
Keyword(s):  
Platelet Aggregation ◽  
Cardiovascular Diseases ◽  
Acetylsalicylic Acid ◽  
Antioxidant Properties ◽  
Benzimidazole Derivatives ◽  
Antioxidant Action ◽  
Antiplatelet Activity ◽  
Reference Drug ◽  
Phenolic Group

Introduction: Cardiovascular diseases are currently the leading cause of global disability and mortality. According to the centers for disease control and prevention, the average life expectancy of a person would be 10 years longer but for a high prevalence of cardiovascular diseases, and if antiplatelet drugs and special therapy were used. Materials and methods: Antiplatelet activity of the novel benzimidazole derivatives containing a sterically hindered phenolic group in their structure has been investigated in vitro, using a model of ADP-induced platelet aggregation of rabbit’s plasma. The compounds exhibiting high antiplatelet activity and acetylsalicylic acid, as a reference drug, were examined for antioxidant properties in an ascorbate-dependent model of lipid peroxidation. Results: It was established that the compounds with high antiplatelet activity demonstrated the pronounced antioxidant action. The compound RU-1144 (1-(3,5-ditretbutyl-4-hydroxyphenyl) -1-hydroxypropyl)-phenyl-pyrimidobenzimidazole hydrochloride), in in vitro experiments, had a pronounced antiplatelet activity, surpassing the reference drug acetylsalicylic acid by 21.8 times; in the study of antioxidant activity, the leader compound was inferior to the reference drug dibunol by 1.7 times. By inhibiting intravascular platelet aggregation in vivo, this compound exceeded acetylsalicylic acid by 1.5 times and was slightly inferior to clopidogrel by 1.4 times. Discussion: Benzimidazole derivatives with a hindered phenolic substituent in their structure exhibited antiplatelet and antioxidant properties. It was established that the compounds with high antiplatelet activity demonstrated the pronounced antioxidant action. Conclusion: The chemical class of benzimidazole derivatives with a hindered phenolic substituent in their structure is promising for the search for new antiaggregant and antioxidant drugs.

Effects of Acetylsalicylic Acid on Inhibition of Ex Vivo Platelet Aggregation and Secretion by SKF 107260, a Novel GPIIb/IIIa Receptor Antagonist

1994 ◽  
Vol 72 (04) ◽  
pp. 622-626 ◽  
Author(s):  
Martin I Freed ◽  
Steven Boike ◽  
Nevine Zariffa ◽  
Diane K Jorkasky
Keyword(s):  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Whole Blood ◽  
Ex Vivo ◽  
Atp Release ◽  
Blood Platelet ◽  
Inhibition Of Platelet Aggregation ◽  
Dependent Inhibition ◽  
Platelet Secretion

SummarySKF 107260 is a potent pentapeptide antagonist of the platelet membrane glycoprotein receptor GP IIb/IIIa. The in vitro platelet inhibitory effects of SKF 107260, acetylsalicylic acid (ASA), and their combination, on collagen-induced platelet aggregation and secretion (ATP release) were assessed in human whole blood. Additionally, the con-centration-response relationships for these inhibitors were compared for males and females in order to explore gender differences in platelet responsiveness. SKF 107260 caused a concentration-dependent inhibition of platelet aggregation which was significant at concentrations ≥30 nM. ASA also caused a concentration-dependent inhibition of platelet aggregation which was significant at concentrations ≥ 1 mg/dl. The addition of ASA 1 mg/dl to increasing concentrations of SKF 107260 resulted in a more pronounced inhibition of platelet aggregation than when either agent was used alone. These data suggest a pharmacologic interaction, especially at SKF 107260 concentrations ≤30 nM. Since ATP release was significantly inhibited at concentrations ≥ 1 nM, platelet secretion appears to be more sensitive than aggregation to inhibition by SKF 107260. These data suggest that platelet secretion in response to collagen is dependent on the aggregation response mediated by GP IIb/IIIa. In conclusion, SKF 107260 is a potent inhibitor of both whole blood platelet aggregation and secretion and these anti-aggregatory effects may be augmented by concomitant ASA administration.

scholarly journals Virgin olive oil polyphenol hydroxytyrosol acetate inhibits in vitro platelet aggregation in human whole blood: comparison with hydroxytyrosol and acetylsalicylic acid

2008 ◽  
Vol 101 (8) ◽  
pp. 1157-1164 ◽  
Author(s):  
José Antonio González Correa ◽  
Juan Antonio López-Villodres ◽  
Rocío Asensi ◽  
José Luis Espartero ◽  
Guillermo Rodríguez-Gutiérez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Olive Oil ◽  
Whole Blood ◽  
Virgin Olive Oil ◽  
Nitric Oxide Production ◽  
Human Whole Blood ◽  
Platelet Thromboxane

Hydroxytyrosol acetate (HT-AC) is a polyphenol present in virgin olive oil (VOO) at a proportion similar to hydroxytyrosol (HT) (160–479 μmol/kg oil). The present study was designed to measure the in vitro platelet antiaggregating activity of HT-AC in human whole blood, and compare this effect with that of HT and acetylsalicylic acid (ASA). The experiments were designed according to the standard procedure to investigate the activity of ASA. HT-AC and HT inhibited platelet aggregation induced by ADP, collagen or arachidonic acid in both whole blood and platelet-rich plasma (PRP). ASA and HT-AC had a greater effect in whole blood than in PRP when ADP or collagen was used as inducer. ASA and HT-AC had a greater effect in PRP+leucocytes than in PRP alone. All three compounds inhibited platelet thromboxane B2 and leucocyte 6-keto-prostaglandin F1α (6-keto-PF1α) production. The thromboxane/6-keto-PGF1α inhibition ratio (as an indirect index of the prostanoid equilibrium) was 10·8 (se 1) for HT-AC, 1·0 (se 0·1) for HT and 3·3 (se 0·2) for ASA. All three compounds stimulated nitric oxide production, although HT was a weaker effect. In our experiments only concentrations higher than 500 μm (HT) or 1 mm (HT-AC and ASA) inhibited 3-nitrotyrosine production. All three compounds inhibited the production of TNFα by leucocytes, with no significant differences between them. In quantitative terms HT-AC showed a greater antiplatelet aggregating activity than HT and a similar activity to that of ASA. This effect involved a decrease in platelet thromboxane synthesis and an increase in leucocyte nitric oxide production.

Changes in platelet function and gastrointestinal bleeding following repeated administration of acetylsalicylic acid in the rat and the dog

1979 ◽  
Vol 57 (3) ◽  
pp. 298-301
Author(s):  
D. G. Mills ◽  
I. J. Lane ◽  
J. D. Otton ◽  
M. A. Cook ◽  
R. B. Philp
Keyword(s):  
Platelet Aggregation ◽  
Blood Loss ◽  
Gastrointestinal Bleeding ◽  
Acetylsalicylic Acid ◽  
Treatment Period ◽  
Platelet Reactivity ◽  
Adenosine Diphosphate ◽  
Repeated Administration ◽  
Standard Techniques

Two dogs were prepared with Pavlov pouches of the fundic area of the stomach using standard techniques. During treatment periods of 14 days, 200 mg acetylsalicylic acid (ASA) was introduced into the pouch twice daily by insufflation. One hour after each drug administration the pouch was washed with saline and the fluid assayed for blood. Bleeding from the pouch increased to a maximum on the 3rd or 4th day of the treatment period and subsequently declined such that by the 8th day blood loss was minimal and approximated that found during control periods. Platelet aggregation (in vitro) responses to adenosine diphosphate were significantly (p < 0.01) inhibited on day 3 when aggregation curve heights were reduced by 66.2 ± 13.11% (mean ± SEM) from control values. On day 7 and during the ensuing 7-day period when ASA was given twice daily, the heights of aggregation responses were reduced by only 20–30% from controls. These responses were significantly (p < 0.001) greater than those found on day 3. Similar changes in platelet reactivity were found in plasma from rats given ASA twice daily for 7 days. Aggregation responses to collagen were depressed by 95.5 ± 4.49% on day 1 following two doses of ASA. As the treatment period continued, the aggregation responses increased in magnitude until the 7th day they were similar in height to those from control animals. The mechanism involved in this adaptation to ASA treatment seen with these platelets is not known.

Effects of Acetylsalicylic Acid on Human Platelet Function In Vivo at Salicylate Steady State

1984 ◽  
Vol 51 (02) ◽  
pp. 269-271 ◽  
Author(s):  
R Simrock ◽  
A Missalla ◽  
P Schwidtal ◽  
V Lischke ◽  
H K Breddin
Keyword(s):  
Steady State ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Human Platelet ◽  
Shape Change ◽  
Clinical Importance ◽  
Tissue Extract ◽  
Platelet Shape

SummaryThe results of clinical trials concerning the use of acetylsalicylic acid (ASA) as antithrombotic drug are contradictory. Inhibition by ASA of platelet prostaglandin synthesis and aggregation is prevented by its metabolite salicylic acid (SA) in animals and in human platelets in vitro. It was suggested that ASA might produce its own inhibitor, thereby diminishing its efficiency in thromboembolic disease.In four healthy male subjects there was no difference in inhibition of collagen-induced platelet aggregation after the administration of 500 mg ASA alone or at salicylate steady state (3 g SA daily). But the inhibition of tissue-extract-induced platelet shape change was diminished and shortened by pretreatment with SA. We conclude that SA does not inhibit the effects of ASA on human platelet aggregation in vivo in therapeutic dose ranges. The clinical importance of the SA/ASA-interaction on tissue-extract-induced platelet shape change remains to be clarified.

Desmopressin Effect on Acetylsalicylic Acid Impaired Platelet Punction

1995 ◽  
Vol 21 (S 02) ◽  
pp. 32-39 ◽  
Author(s):  
Karl-Heinz Beck ◽  
Patrick Mohr ◽  
Ulrich Bleckmann ◽  
Hermann Schweer ◽  
Volker Kretschmer
Keyword(s):  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Bleeding Time ◽  
Direct Interaction ◽  
Inverse Correlation ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Antigen

The mechanism of DDAVP's shortening of acetylsalicylic acid (ASA) prolonged bleeding times was investigated. Sixteen healthy subjects received two dosages of ASA (100 mg) in 12 hours. Twenty four hours after the first ASA application and again after 32 hours DDAVP was administered intravenously (0.4 μLg/kg). The trial was terminated after 48 hrs. In between, blood samples were drawn and analyzed for the in vivo bleeding time (Simplate® time), in vitro bleeding test (IVBT, Thrombostat 4000), von Willebrand factor antigen (vWf:Ag), Ristocetin cofactor activity (vWf R:Co), plasma β-thromboglobulin (β-TG), platelet ATP/ADP, platelet aggregation (collagen, ADP, arachidonic acid), and plasma and platelet thromboxane levels. Simplate ® time (BT) and IVBT showed an excellent inverse correlation with vWf R:Co (r2 BT = 0.97 and r2 1VBT = 0.99, respectively) during the time when DDAVP was administered, suggesting the involvement of plasma vWF in DDAVP's shortening of the bleeding time. The involvement of plasma thromboxane in this mechanism could be excluded. In addition, DDAVP hampered platelet aggregation tests, possibly due to the inhibition of the release reaction (reduced β-TG in plasma) by a direct interaction with platelets.

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