Mean platelet volume: Interrelation with platelet aggregation activity and glycoprotein IIb-IIIa and Ib expression levels

Хаспекова, С. Г.; Zyuryaev, I T; Yakushkin, V. V.; Naimushin, Ya. A.; Сироткина, О. В.; Zaytseva, N. O.; Ruda, Mikhail; Мазуров, А. В.

doi:10.1134/s199075081402005x

Cited by 5 publications

(3 citation statements)

References 31 publications

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“…All antiplatelet agents used in the study were tested for their ability to inhibit platelet aggregation. Platelet aggregation in PRP was recorded using the standard turbidimetric method in a BIOLA aggregation analyzer (BIOLA, Moscow, Russia) as described previously [26]. PRP was not treated with platelet inhibitors (control) or treated with 0.2 mM ASA (Sigma-Aldrich, St. Louis, MO, USA), 1 µM ticagrelor (Sigma-Aldrich, MO), 20 µg/mL ruciromab (F(ab)2 fragment of ant-GP IIb-IIIa monoclonal antibody FRaMon (CRC64)) (Framon Ltd., Moscow, Russia), or 1 µg/mL PGE1 (Sigma-Aldrich, MO) for 5 min at 37 • C. For ASA testing, aggregation was induced by 1 mM arachidonic acid (Santa Cruz Biotechnology, Heidelberg, Germany), for ticagrelor testing, by 20 µM ADP (AppliChem GmbH, Darmstadt, Germany), and for ruciromab and PGE1 testing, by 20 µM TRAP (sequence SFLLRN, provided by Dr. M.D.…”

Section: Platelet Aggregationmentioning

confidence: 99%

Effects of Antiplatelet Drugs on Platelet-Dependent Coagulation Reactions

et al. 2023

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Activated platelets are involved in blood coagulation by exposing phosphatidylserine (PS), which serves as a substrate for assembling coagulation complexes. Platelets accelerate fibrin formation and thrombin generation, two final reactions of the coagulation cascade. We investigated the effects of antiplatelet drugs on platelet impact in these reactions and platelet ability to expose PS. Washed human platelets were incubated with acetylsalicylic acid (ASA), ticagrelor, ASA in combination with ticagrelor, ruciromab (glycoprotein IIb-IIIa antagonist), or prostaglandin E1 (PGE1). Platelets were not activated or activated by collagen and sedimented in multiwell plates, and plasma was added after supernatant removal. Fibrin formation (clotting) was monitored in a recalcification assay by light absorbance and thrombin generation in a fluorogenic test. PS exposure was assessed by annexin V staining using flow cytometry. Ticagrelor (alone and in combination with ASA), ruciromab, and PGE1, but not ASA, prolonged the lag phase and decreased the maximum rate of plasma clotting and decreased the peak and maximum rate of thrombin generation. Inhibition was observed when platelets were not treated with exogenous agonists (activation by endogenous thrombin) and pretreated with collagen. Ticagrelor (alone and in combination with ASA), ruciromab, and PGE1, but not ASA, decreased PS exposure on washed platelets activated by thrombin and by thrombin + collagen. PS exposure on activated platelets in whole blood was lower in patients with acute coronary syndrome receiving ticagrelor + ASA in comparison with donors free of medications. These results indicate that antiplatelet drugs are able to suppress platelet coagulation activity not only in vitro but also after administration to patients.

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Section: Platelet Aggregationmentioning

confidence: 99%

Effects of Antiplatelet Drugs on Platelet-Dependent Coagulation Reactions

et al. 2023

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“…All antiplatelet agents used in the study were tested for their ability to inhibit platelet aggregation. Platelet aggregation in PRP was recorded using standard turbidimetric method in a BIOLA aggregation analyzer (BIOLA, Russia ) as described previously [26]. PRP was left intact or supplemented with 0.2 mM ASA (Sigma-Aldrich, Saint Louis, MO), 1 µM ticagrelor (Sigma-Aldrich, Saint Louis, MO USA), 20 µg/ml ruciromab (F(ab)2 fragment of ant-GP IIb-IIIa monoclonal antibody FRaMon (CRC64)) (Mona Ltd, Moscow) or 1 µg/ml PGE1 (Sigma-Aldrich, Saint Louis, MO) and incubated for 5 min at 37 o C. For ASA testing aggregation was induced by 1 mM arachidonic acid (Santa Cruz Biotechnology Heidelberg, Germany), for ticagrelor testing, by 20 µM ADP (AppliChem GmbH, Darmstadt, Germany) and for ruciromab and PGE1 testing, by 20 µM TRAP (sequence SFLLRN, provided by Dr. M.D.…”

Section: Platelet Aggregationmentioning

confidence: 99%

Effects of Antiplatelet Drugs on Platelet-Dependent Coagulation Reactions

Muravlev¹,

Dobrovolsky²,

Антонова³

et al. 2023

Preprint

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Activated platelets are involved in blood coagulation by exposing phosphatidylserine (PS), which serves as a substrate for assembling coagulation complexes. Platelets accelerate fibrin formation and thrombin generation, two final reactions of the coagulation cascade. We investigated the effects of antiplatelet drugs on platelet impact in these reactions and platelet ability to expose PS. Washed human platelets were incubated with acetylsalicylic acid (ASA), ticagrelor, ASA in combination with ticagrelor, ruciromab (glycoprotein IIb-IIIa antagonist) or prostaglandin E1 (PGE1). Platelets were not activated or activated by collagen, sedimented in multiwell plates and plasma was added after supernatant removal. Fibrin formation (clotting) was monitored in a recalcification assay by light absorbance and thrombin generation in a fluorogenic test. PS exposure was assessed by annexin V staining using flow cytometry. Ticagrelor (alone and in combination with ASA), ruciromab and PGE1, but not ASA prolonged the lag phase and decreased the maximum rate of plasma clotting, and decreased the peak and maximum rate of thrombin generation. Inhibition was observed when platelets were not treated with exogenous agonists (activation by endogenous thrombin) and pretreated with collagen. Ticagrelor (alone and in combination with ASA), ruciromab and PGE1, but not ASA decreased PS exposure on washed platelets activated by thrombin and by thrombin + collagen. PS exposure on activated platelets in whole blood was lower in patients with acute coronary syndrome receiving ticagrelor + ASA in comparison with donors free of medications. These results indicate that antiplatelet drugs are able to suppress platelet coagulation activity not only in vitro but also after administration to patients.

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“…13 Adapun faktor perancu yang mungkin mempengaruhi dari nilai MPV yaitu adanya onset dari STEMI yang homogen, dimana dalam kaitannya dengan kejadian trombosis yang melibatkan proses agregasi platelet, menurut penelitian dari Khaspekova dkk, (2014) dimana dengan menggunakan sampel pasien dengan ACS sebanyak 116 dan pasien sehat/kontrol sebanyak 38 orang didapatkan bahwa dengan dilakukannya stimulasi agregasi platelet pada kelompok kontrol dan ACS didapatkan bahwa adanya korelasi yang signifikan antara MPV dengan tingkat agregasi platelet pada kedua kelompok. 14 Selain itu faktor perancu yang mungkin mempengaruhi hasil perhitungan luas infark miokard pada penelitian ini yaitu obatobatan. Dimana obat-obatan tersebut digunakan oleh pasien dengan riwayat hipertensi yang termasuk di dalam subjek penelitian ini.…”

Section: Pembahasanunclassified

Hubungan Antara MPV (Mean Platelet Volume) Dengan Luas Infark Miokard Pada Pasien Stemi (St-Segment Elevated Myocardial Infarction) Yang Diukur Berdasarkan Skor QRS Selvester

Bagus Kantwa Abhimantra,

Rahmat,

Pintaningrum

2022

eum

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Background: Globally heart disease occupy the first order of mortality population in the world. Acute myocardial infarction is one of them, in its classification AMI can be divided into STEMI and NSTEMI. Pathological changes in AMI will involve many things, one of them is platelets. The aim of the study is to know the correlation between Mean Platelet Volume (MPV) and the myocardial infarction size in STEMI patient based on QRS Selvester score. Methods: This study was an observational analytic study with a cross sectional approach. This research was conducted in July 2020-March 2021 at the Rumah Sakit Umum Kota Mataram, involving 63 subjects. Data obtained from patient medical records using non-probability sampling technique which is consecutive sampling. Results: From 63 data, there are 50 male patients and 13 female patients, the average of the patients age is 57.97 years old. MPV mean is 8.77 fL and the mean of myocardial infarction size is 25.33%. The data scale of the two variables is numerical for MPV and numerical for the myocardial infarction size. The normality test was performed using the Kolmogorov-Smirnov test and the MPV significance value was 0.200 and the myocardial infarction size was 0.200 (normal distribution). Pearson correlation test results obtained p=0.885 (p> 0.05). Conclusion: There is no significant correlation between the MPV and the myocardial infarction size.

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Mean platelet volume: Interrelation with platelet aggregation activity and glycoprotein IIb-IIIa and Ib expression levels

Cited by 5 publications

References 31 publications

Effects of Antiplatelet Drugs on Platelet-Dependent Coagulation Reactions

Effects of Antiplatelet Drugs on Platelet-Dependent Coagulation Reactions

Effects of Antiplatelet Drugs on Platelet-Dependent Coagulation Reactions

Hubungan Antara MPV (Mean Platelet Volume) Dengan Luas Infark Miokard Pada Pasien Stemi (St-Segment Elevated Myocardial Infarction) Yang Diukur Berdasarkan Skor QRS Selvester

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