Mg++ - and Ca++-Induced Platelet Aggregation and ADP

1970 ◽  
Vol 24 (03/04) ◽  
pp. 432-437 ◽  
Author(s):  
S Cronberg ◽  
J. P Caen
Keyword(s):  
Platelet Aggregation ◽  
Pyruvate Kinase ◽  
Pyruvic Acid ◽  
Active Principle ◽  
Platelet Suspension ◽  
Edta Plasma ◽  
Phosphoenol Pyruvic Acid

SummaryReports on platelet aggregation after addition of calcium or magnesium to EDTA- PRP or platelet suspensions were confirmed. An aggregating principle was found in the EDTA-plasma and the supernatant of the platelet suspensions. Aggregation by magnesium in a platelet suspension was inhibited by adenosine and phosphoenol- pyruvic acid and pyruvate kinase, which suggested that the active principle was identical with ADP. Degradation of ADP in EDTA plasma was blocked.It thus appears that aggregation induced by calcium or magnesium in EDTA-PRP and platelet suspension was due to accumulation of spontaneously liberated ADP, which was not degraded.

Inhibitory Effect of Staphylokinase on Platelet Aggregation

1993 ◽  
Vol 70 (05) ◽  
pp. 834-837 ◽  
Author(s):  
Akira Suehiro ◽  
Yoshio Oura ◽  
Motoo Ueda ◽  
Eizo Kakishita
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Degradation Products ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Effective Concentration ◽  
Inhibit Platelet Aggregation ◽  
Platelet Suspension ◽  
Washed Platelet ◽  
Human Platelet Aggregation

SummaryWe investigated the effect of staphylokinase (SAK), which has specific thrombolytic properties, on human platelet aggregation. Platelet aggregation induced with collagen was observed following preincubation of platelets in platelet-rich plasma (PRP) or washed platelet suspension (WP) with SAK at 37° C for 30 min. SAK inhibited platelet aggregation in PRP only at the highest examined concentration (1 x 10-4 g/ml). Although SAK did not inhibit platelet aggregation in WP which contained fibrinogen, it did when the platelets had been preincubated with SAK and plasminogen. The most effective concentration in WP was 1 x 10-6 g/ml. The effect could be inhibited by adding aprotinin or α2-antiplasmin. The highest generation of plasmin in the same preincubation fluid was detected at 1 x 10-6 g/ml SAK. We concluded that SAK can inhibit platelet aggregation in WP by generating plasmin and/or fibrinogen degradation products, but is only partially effective in PRP because of the existence of α2-antiplasmin.

scholarly journals Screening Test for Platelet Aggregation Inhibitor in Natural Products. The Active Principle of Anemarrhenae Rhizoma

1988 ◽  
Vol 108 (6) ◽  
pp. 555-561 ◽  
Author(s):  
AKIRA NIWA ◽  
OSAMU TAKEDA ◽  
MASAKO ISHIMARU ◽  
YASUKO NAKAMOTO ◽  
KAZUO YAMASAKI ◽  
...  
Keyword(s):  
Natural Products ◽  
Platelet Aggregation ◽  
Screening Test ◽  
Active Principle ◽  
Platelet Aggregation Inhibitor ◽  
Aggregation Inhibitor

scholarly journals New Method for Assessment of Plasma Von Willebrand Factor

1977 ◽  
Author(s):  
T. Sano ◽  
T. Motomiya ◽  
N. Mashimo ◽  
H. Yamazaki
Keyword(s):  
Platelet Aggregation ◽  
Von Willebrand Factor ◽  
Platelet Rich Plasma ◽  
Normal Subjects ◽  
Induce Platelet Aggregation ◽  
Platelet Suspension ◽  
Maximal Plasma ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Diabetes Melitus

As much interests have been focused on von Willebrand factor (vWF) in diabetes melitus and atherosclerosis, request to determine vWF has been increasing recently. Two methods for assessment of plasma vWF level, without platelet aggregometer, were devised. 1) Platelet-rich plasma (PRP) sensitivity to ristocetin-induced platelet aggregation (RIPA): PRP was separated without centrifugation from citrated blood. Serially two-fold diluted restocetin (16 to 16x2-10 mg/ml) was prepared in a Cooke Microtiter tray and PRP (25 μl each) was added to each concentration of ristocetin. Then the ristocetin-PRP mixture was agitated for 15 seconds using a Kowa Kizai Micromixer and the minimum effective final concentration of ristocetin to give platelet aggregation was obtained microscopically and this was defined as PRP sensitivity to RIPA. This method is convenient for screening test. 2) vWF assay:Serially two-fold diluted plasma (2 to 1024 times, in Tris-salin pH 7.2 containing 12 mg/ml bovine serum albumin), fixed and washed platelet suspension (6x105 /μl, Macfarlane et al.1975) and 3 mg/ml ristocetin were mixed (25 μl each) in a microtiter tray and agitated for 15 seconds. The maximal plasma dilution to induce platelet aggregation was obtained microscopically and defined as the titer of plasma vWF. In normal subjects, minimum effective ristocetin concentration (PRP sensitivity to RIPA) was around 1 to 0.5 mg/ml and maximal plasma dilution to give platelet aggregation (vWF titer) was around 16 to 32 times. The present methods have a good reproducibility and are performed easily without aggregometer and thought to be useful clinically.

scholarly journals A potent antiplatelet peptide, triflavin, from Trimeresurus flavoviridis snake venom

1991 ◽  
Vol 277 (2) ◽  
pp. 351-357 ◽  
Author(s):  
T F Huang ◽  
J R Sheu ◽  
C M Teng
Keyword(s):  
Platelet Aggregation ◽  
Snake Venom ◽  
Ionic Exchange ◽  
Dependent Manner ◽  
Single Chain ◽  
Platelet Suspension ◽  
Trimeresurus Flavoviridis ◽  
Platelet Membranes ◽  
Fibrinogen Binding ◽  
Induced Aggregation

The interaction of fibrinogen with its receptors on platelet surfaces leads to platelet aggregation. A snake-venom peptide, trigramin, has previously been demonstrated to inhibit platelet aggregation by acting as a fibrinogen-receptor antagonist. By means of gel filtration, ionic-exchange chromatography and reverse-phase h.p.l.c., a potent platelet-aggregation inhibitor, triflavin, has now been purified from the venom of Trimeresurus flavoviridis. The purified triflavin is a single-chain polypeptide, consisting of about 71 amino acid residues with a molecular mass of 7600 Da, and its N-terminal sequence is Gly-Glu-Glu-Cys-Asp. Triflavin dose-dependently inhibited human platelet aggregation stimulated by ADP, adrenaline, collagen, thrombin or prostaglandin endoperoxide analogue U46619 in preparations of platelet-rich plasma, platelet suspension and whole blood. Its IC50 ranged from 38 to 84 nM, depending on the aggregation inducer used and the platelet preparation. However, triflavin apparently did not affect the platelet shape change and ATP-release reactions caused by these agonists. Triflavin inhibited fibrinogen-induced aggregation of human elastase-treated platelets in a dose-dependent manner, indicating that it directly interferes with the binding of fibrinogen to its receptors on platelet membranes exposed by elastase treatment. Additionally, triflavin dose-dependently blocked 125I-labelled fibrinogen binding to ADP-activated platelets. In conclusion, triflavin inhibits platelet aggregation through the blockade of fibrinogen binding to fibrinogen receptors on platelet membranes.

scholarly journals The effect of centrifugation speed and time on pre-analytical platelet activation

2016 ◽  
Vol 54 (12) ◽  
Author(s):  
Anna C. Söderström ◽  
Mads Nybo ◽  
Christian Nielsen ◽  
Pernille J. Vinholt
Keyword(s):  
Platelet Aggregation ◽  
Healthy Volunteers ◽  
Platelet Activation ◽  
Platelet Rich Plasma ◽  
Cell Content ◽  
Median Percentage ◽  
Handling Stress ◽  
Edta Plasma ◽  
Edta Anticoagulated Blood

AbstractBackground:The results of laboratory analyses are affected by pre-analytical variables, and in particular can platelets be activated by shear handling stress and secrete granular substances. We therefore evaluated the effect of centrifugation speed and time on pre-analytical platelet activation.Methods:Citrate- and EDTA-anticoagulated blood from healthy volunteers were centrifuged at 80–10,000Results:The median percentage of platelets expressing P-selectin in citrate- and EDTA-plasma centrifuged at 2000Conclusions:Proportional to centrifugation speed, platelets in plasma and platelet-rich plasma were activated with centrifugation speed, cell content and composition changed while platelet aggregation was unaltered.

ChemInform Abstract: Towards a Synthesis of Glucidic Phosphoenol Pyruvic Acid Derivatives.

ChemInform ◽  
2010 ◽  
Vol 30 (34) ◽  
pp. no-no
Author(s):  
Philippe Coutrot ◽  
Claude Grison ◽  
Mohamed Tabyaoui ◽  
Badia Tabyaoui ◽  
Stephane Dumarcay
Keyword(s):  
Pyruvic Acid ◽  
Phosphoenol Pyruvic Acid

scholarly journals Use of increased concentrations of adenosinediphosphate for high residual platelet reactivity in patients with coronary heart disease

2021 ◽  
Vol 70 (1) ◽  
pp. 129-132
Author(s):  
O.A. Trubacheva ◽  
S.N. Belyaeva ◽  
T.E. Suslova ◽  
I.V. Petrova
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Transmission Curve ◽  
Platelet Suspension

Detection of a tendency to increased thrombosis in patients with coronary heart disease (CHD) is of important prognostic value in the selection of drugs aimed at achieving a persistent antithrombotic effect. The aim of the study was to evaluate the use of elevated ADP inducer concentrations to improve the accuracy of ADP-induced platelet aggregation in patients with coronary heart disease. Material and method. Material and method. We studied 48 patients with CHD who were on continuous double antiplatelet therapy for 6 months (aspirin 75mg and clopidogrel 75mg per day). The aggregation activity of the platelet suspension was studied using the Born method G. in the modification of Gabbasov Z. A. Platelet activity was evaluated by the degree of aggregation of platelet-rich plasma along the light transmission curve under the influence of the inducer adenosine diphosphate (ADP) at a concentration of 2 mmol/l and by its own patented method against the background of additional ADP application. Results. In patients, platelet aggregation decreased to 5-35% (p<0.005) compared to the standard values, which are 50-60%. The values of platelet aggregation with the additional introduction of the inducer of aggregation ADP in a ratio of 2:1 to 2 µmol/l for 1, 2, 3, and 4-minute registration of platelet aggregation, resulted in increased aggregation from 55% to 75% (p<0.001), indicating high residual platelet reactivity on the background of double antiplatelet therapy. Correlations of the degree of aggregation for elevated ADP concentrations with multivessel arterial lesion and dyslipidemia were also found, r=0.86 and r=0.92, respectively. Conclusion. The use of elevated concentrations of adenosine diphosphate in platelet aggregation in patients with ischemic heart disease increases the accuracy of assessing ADP-induced platelet aggregation against the background of dual antiplatelet therapy and contributes to the detection of high residual platelet reactivity.

Localization of Inhibition of Platelet Aggregation by Incubation of Platelet Rich EDTA-Plasma at 37°C

1968 ◽  
Vol 19 (01/02) ◽  
pp. 001-011 ◽  
Author(s):  
R Gross ◽  
G Niemeyer ◽  
H Reuter
Keyword(s):  
Platelet Aggregation ◽  
Inhibitory Substance ◽  
Inhibition Of Platelet Aggregation ◽  
Edta Plasma

SummaryBy photometric and microscopic technics investigations have been carried out to determine the nature of the inhibition of platelet aggregation caused by incubating platelet rich EDTA-plasma at 37° C. The results clearly indicate that the inhibition must arise from alterations in the platelets themselves. The appearance of an inhibitory substance in plasma and the release of such a substance from the platelets into the plasma have been excluded. Addition of ADP to the inhibited platelets did not influence the inhibition of platelet aggregation.

scholarly journals PLATELET PHAGOCYTOSIS AND AGGREGATION

1965 ◽  
Vol 27 (3) ◽  
pp. 531-543 ◽  
Author(s):  
Henry Z. Movat ◽  
William J. Weiser ◽  
Michael F. Glynn ◽  
James F. Mustard
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Chelating Agent ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
Inhibit Platelet Aggregation ◽  
Platelet Suspension ◽  
Latex Particles ◽  
Washed Platelet

The addition of latex particles to native (no anticoagulant) or citrated human platelet-rich plasma (PRP), or to a once-washed platelet suspension causes platelet aggregation. This aggregation is associated with phagocytosis of the latex particles by the platelets and appears to be due to release of adenosine diphosphate (ADP) from the platelets. Adenosine and adenosine monophosphate, which are known to inhibit platelet aggregation induced by ADP, also block that induced by latex. These compounds do not prevent the phagocytosis of latex particles by the platelet. The addition of iodoacetate and 2,4-dinitrophenol in appropriate concentrations to the PRP, prior to the addition of the latex, blocks platelet aggregation and phagocytosis. This is also true for the chelating agent ethylenediaminetetraacetate (EDTA). Platelets left in contact with latex for a sufficient period of time show loss of their granules. Leucocytes phagocytose both latex and platelets that had themselves phagocytosed latex. It is concluded that phagocytosis of latex particles by platelets resembles that by white cells, and that in both processes metabolic changes appear to be involved.

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