Effects of Dextrans on Some Platelet Functions

2015 ◽  
pp. 1140-1140
Author(s):  
R. Eliasson ◽  
S. Bygdeman
Keyword(s):  
Platelet Functions

Effects of Bupranolol, a New β-Blocker, on Platelet Functions of Rabbit and Human in Vitro

1976 ◽  
Vol 36 (02) ◽  
pp. 376-387 ◽  
Author(s):  
Teruhiko Umetsu ◽  
Kazuko Sanai ◽  
Tadakatsu Kato
Keyword(s):  
Platelet Aggregation ◽  
Platelet Adhesion ◽  
Human Platelets ◽  
Rabbit Platelet ◽  
Rabbit Platelets ◽  
Β Blocker ◽  
Platelet Aggregates ◽  
Induced Aggregation ◽  
Platelet Functions

SummaryThe effects of bupranolol, a new β-blocker, on platelet functions were investigated in vitro in rabbits and humans as compared with propranolol, a well-known β-blocker. At first, the effect of adrenaline on ADP-induced rabbit platelet aggregation was studied because adrenaline alone induces little or no aggregation of rabbit platelets. Enhancement of ADP-induced rabbit platelet aggregation by adrenaline was confirmed, as previously reported by Sinakos and Caen (1967). In addition the degree of the enhancement was proved to be markedly affected by the concentration of ADP and to increase with decreasing concentration of ADP, although the maximum aggregation (percent) was decreased.Bupranolol and propranolol inhibited the (adrenaline-ADP-)induced aggregation of rabbit platelets, bupranolol being approximately 2.4–3.2 times as effective as propranolol. Bupranolol stimulated the disaggregation of platelet aggregates induced by a combination of adrenaline and ADP, but propranolol did not. Platelet adhesion in rabbit was also inhibited by the β-blockers and bupranolol was more active than propranolol. With human platelets, aggregation induced by adrenaline was inhibited by bupranolol about 2.8–3.3 times as effectively as propranolol.From these findings. We would suggest that bupranolol might be useful for prevention or treatment of thrombosis.

Effects of Halothane on Platelet Function

1980 ◽  
Vol 44 (03) ◽  
pp. 143-145 ◽  
Author(s):  
J Dalsgaard-Nielsen ◽  
J Gormsen
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Platelet Rich Plasma ◽  
Human Platelets ◽  
Halothane Anaesthesia ◽  
Inhibition Of Platelet Aggregation ◽  
Transient Impairment ◽  
High Concentrations ◽  
Uptake And Release ◽  
Platelet Functions

SummaryHuman platelets in platelet rich plasma (PRP) incubated at 37° C with 0.3–2% halothane for 5–10 min lost the ability to aggregate with ADP, epinephrine and collagen.At the same time uptake and release of 14C-serotonin was inhibited. When halothane supply was removed, platelet functions rapidly returned to normal. However, after high concentrations of halothane, the inhibition of platelet aggregation was irreversible or only partially reversible.The results suggest that halothane anaesthesia produces a transient impairment of platelet function.

Platelet Functions in Relation to Dietary Fats in Farmers from two Regions of France

1978 ◽  
Vol 40 (02) ◽  
pp. 518-531 ◽  
Author(s):  
S Renaud ◽  
E Dumont ◽  
F Godsey ◽  
A Suplisson ◽  
C Thevenon
Keyword(s):  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Plasma Cholesterol ◽  
Phospholipid Composition ◽  
Saturated Fat ◽  
Phosphatidyl Inositol ◽  
Phosphatidyl Serine ◽  
Dietary Fats ◽  
Platelet Phospholipid ◽  
Platelet Functions

SummaryTo determine whether the long-term feeding of dietary fats affect platelet functions in man, platelet aggregation (to thrombin ADP, collagen, epinephrine) and clotting activity of platelet-rich plasma (PRP), platelet-poor plasma and of washed platelets, were studied in a mobile-laboratory in 44 healthy male farmers (40-45 years) from two French regions Var and Moselle, in relation to lipemia, glycemia, dietary nutriments, and platelet phospholipid composition. In the Moselle subjects, the platelet clotting activity of PRP and of washed platelets, the platelet aggregation to thrombin and ADP, were highly significantly (p <0.001) increased as compared to those of Var, but not the plasma cholesterol, which was identical in the two regions.In Moselle, the intake of total calories, total lipids and saturated fats was higher than in the Var.However, it was only with the saturated fat intake (mostly stearic acid) that the platelet clotting activity (p <0.01) and the platelet aggregation (p <0.001) were highly significantly correlated. The platelet clotting activity was also significantly (p <0.001) correlated with the fatty acid composition of the platelet phospholipid fractions phosphatidyl serine + phosphatidyl inositol.

Daunorubicin and Platelet Function

1981 ◽  
Vol 45 (01) ◽  
pp. 038-042 ◽  
Author(s):  
M E Pogliani ◽  
R Fantasia ◽  
G Lambertenghi-Deliliers ◽  
E Cofrancesco
Keyword(s):  
Electron Microscope ◽  
Cellular Membrane ◽  
Hemorrhagic Diathesis ◽  
Clot Retraction ◽  
Freezing And Thawing ◽  
Platelet Factor ◽  
High Doses ◽  
Very High ◽  
Platelet Functions

SummaryThe influence of Daunorubicin on some platelet functions in vitro was investigated, using different concentrations of the drug (0.01-0.02-0.04 μg/ml). Daunorubicin was shown to inhibit Collagen and Thrombin induced platelet aggregation and the intensity of inhibition depended on both drug concentration and the time of preincubation.Daunorubicin was also shown to inhibit the release reaction, the platelet prostaglandin pathway and the availability platelet factor 3; the drug at concentrations for clinical use does not damage the platelet membrane, as is the case with the freezing and thawing test, in platelet uptake of 14C-serotonin and as confirmed by the electron microscope. When very high doses (0.16 mg) of Daunorubicin are used, lysis of the platelets can be observed and this is confirmed under the electron microscope by the presence of empty platelets with fractures at the level of the cytoplasmic membrane.Finally, Daunorubicin causes irreversible inhibition of reptilase clot-retraction, even if this is less severe than with Vincristine. Working with gel-filtered platelets, it would appear that the inhibition exercised by the drug on platelet reactions is not caused through modifications in Ca++ metabolism.The authors suggest that Daunorubicin, at the dosages used clinically, induces in vitro thrombocytopathy without damaging the cellular membrane as confirmed by the electron microscope.This impairment of platelet functions could play a part in hemorrhagic diathesis observed during Daunorubicin therapy.

The Effect of Adenosine Phosphates on the Spreading of Normal Human Platelets

1969 ◽  
Vol 21 (02) ◽  
pp. 373-379
Author(s):  
H Linker ◽  
H Reuter
Keyword(s):  
Human Platelets ◽  
Adenosine Phosphates ◽  
Normal Human ◽  
Platelet Functions

SummaryThe spreading of human platelets requires the presence of ADP as do other platelet functions. In the plasma of patients with a failure of release of ADP from the platelets the also decreased ability to spread can be normalized by exogenous ADP. AMP and ATP inhibit the spreading of platelets.

NADPH-Oxidase in Paracrine and Autocrine Regulation of Platelet Functions

2015 ◽  
Vol 6 (1) ◽  
pp. 79-90
Author(s):  
Sergii A. Talanov ◽  
Tatjana I. Lyashenko ◽  
Irina I. Patalakh
Keyword(s):  
Nadph Oxidase ◽  
Autocrine Regulation ◽  
Platelet Functions

EFFECT OF DDAVP ON PRIMARY HEMOSTASIS WITH CONGENITAL AFIBRINOGENEMIA

1987 ◽  
Author(s):  
M Taki ◽  
M Inagaki ◽  
T Miura ◽  
N Saito ◽  
T Meguro ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Retention Rate ◽  
Platelet Membrane ◽  
Bleeding Tendency ◽  
Primary Hemostasis ◽  
Prolonged Bleeding Time ◽  
Before And After ◽  
Congenital Afibrinogenemia ◽  
Von Willebrand ◽  
Platelet Functions

It has been reported recently that DDAVP might be an useful tool in the therapy and prevention of bleeding in patients with congenital afibrinogenemia (CA).To study the mechanism of its efficacy, changes in the platelet functions of a patient with CA were examined prior to, and one hour after, the infusion of DDAVP (0.4 μg/Kg). A patient with Glanzmann's thrombasthenia (GT) was also examined, to allow a study of the role of platelet membrane glycoprotein IIb/IIIa (GP IIb/IIIa), a deficient platelet in GT, in the resulting effects of the drug. When both patients were infused with DDAVP, the level of plasma von Willebrand factor (vWF) increased two- to fourfold, accompanied by an enhancement of ristocetin-induced platelet agglutination. The level of plasma fibrinogen was never changed.The prolonged bleeding time observed was markedly improved only in the CA patient, remaining unchanged in the GT patient, after the infusion of DDAVP. This indicates that DDAVP is effective in diminishing the bleeding tendency in CA, but not in GT. Among the platelet functions tested, only the platelet retention rate on glass beads, ADP-induced platelet aggregation and collagen-induced platelet aggregation improved in CA, each remaining unchanged in GT. In particular, collagen-induced platelet aggregation was markedly improved in the CA patient. However, the platelet adhesion to collagen (50 μg/ml)-Sepharose remained normal, both before and after the infusion of DDAVP in CA.These results suggest that an increase in the plasma vWF level and the existence of platelet membrane GPIIb/IIIa may be necessary for the improvement of primary hemostasis, after the infusion of DDAVP. The vWF-mediated platelet aggregation by collagen or ADP may produce this effect in the CA patient.

scholarly journals Use of Thromboelastography Platelet Mapping for Assessment of Individual Platelet Response Secondary to Oral Antiplatelet Therapy after Percutaneous Coronary Intervention: An Attempt to Start Personalized Antiplatelet Therapy in India

2021 ◽  
Author(s):  
Suvro Sankha Datta ◽  
Dibyendu De ◽  
Nadeem Afroz Muslim
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Antiplatelet Therapy ◽  
Platelet Reactivity ◽  
Coronary Intervention ◽  
Platelet Inhibition ◽  
P Value ◽  
Platelet Response ◽  
Percutaneous Coronary ◽  
The Individual ◽  
Platelet Functions

AbstractHigh on-treatment platelet reactivity (HPR) with P2Y12 receptor antagonists in patients treated with dual antiplatelet therapy (DAPT) is strongly associated with adverse ischemic events after percutaneous coronary intervention (PCI). This prospective study was conducted to assess individual platelet response and HPR to antiplatelet medications in post-PCI cases by thromboelastography platelet mapping (TEG-PM). Total 82 patients who were on aspirin and on either clopidogrel, prasugrel, or ticagrelor were evaluated. The percentage of platelet inhibition to arachidonic acid (AA) and adenosine disdiphosphate (ADP) was calculated by [100-{(MA ADP/AA–MA Fibrin) / (MA Thrombin–MA Fibrin) × 100}], taking 50% response as cut-off for HPR. HPR to clopidogrel and prasugrel was 14.29 and 12.5%, respectively. No HPR was detected to aspirin and ticagrelor. The mean percentage of platelet inhibition was significantly higher in patients with ticagrelor 82.99, 95% confidence interval (CI) of [77.3, 88.7] as compared with clopidogrel 72.21, 95% CI of [65.3, 79.1] and prasugrel 64.2, 95% CI of [52.5, 75.9] (p-value of 0.041 and 0.003, respectively). Aspirin along with ticagrelor is associated with a higher mean percentage of platelet inhibition, and lower HPR as compared with the usage of aspirin combined with clopidogrel or prasugrel. Additionally, it might also be concluded that TEG-PM could be used effectively to measure the individual platelet functions which would make oral antiplatelet therapy more personalized for cardiac patients.

Disturbance Of Platelet Function In The Nephrotic Syndrome

1981 ◽  
Author(s):  
E Walter ◽  
D Deppermann ◽  
K Andrassy ◽  
E Weber
Keyword(s):  
Nephrotic Syndrome ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Kidney Function ◽  
Platelet Function ◽  
Platelet Adhesiveness ◽  
Spontaneous Aggregation ◽  
Spontaneous Platelet Aggregation ◽  
Platelet Functions

Thromboembolic phenomena often (30 %) complicate the nephrotic syndrome. It was therefor investigated, wether disturbed platelet functions play a role in this disease.28 normals, 34 patients with nephrotic syndrome and 18 of them with impaired kidney function were tested. In 20 patients the measurements were repeated after administration of aspirin plus dipyridamo1e.Patients with nephrotic syndrome showed in comparison to normals the following changes: 1. increased platelet count (p < 0.01), 2. enhanced platelet adhesiveness (Wright-test: p < 0.001), 3. increased spontaneous aggregation (PAT I: p < 0.001; PAT III: p < 0.01), 4. enhanced PF 4-activity (heparin neutralisation: p < 0.001), 5. elevated β TG-levels only in impaired kidney function. There was no difference in the reaction of platelets against ADP as well as collagen. The changes in platelet function correlated with the severity of the nephrotic syndrome (proteinurea, hypalbuminaemia, hyperlipo- proteinaemia). After aspirin plus dipyridamole administration spontaneous platelet aggregation and adhesiveness were normalized.There is a disturbance of platelet function in patients with nephrotic syndrome, which can be reversed with antiaggregating agents.

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