Effect of Acetyl Salicylic Acid on Platelet Function in Yivo

1975 ◽  
Author(s):  
A. A. Hassanein ◽  
N. Afifi ◽  
M. Badr
Keyword(s):  
Salicylic Acid ◽  
Single Dose ◽  
Platelet Aggregation ◽  
Inhibitory Effect ◽  
Acetyl Salicylic Acid ◽  
Clotting Time ◽  
Significant Prolongation ◽  
Platelet Disaggregation ◽  
Platelet Release ◽  
Coagulation Pathway

The ingestion of a single dose of 300 mg. acetyl salicylic acid (ASA) cause after two hours, significant diminution in ADP-induced platelet aggregation and increase in platelet disaggregation. The calcium-induced platelet aggregation test, a turbidimetric modification of the Chandler tube technique, showed significant prolongation in the onset of aggregation and in the clotting time. A test based on the contact product forming activity of platelets showed inhibition after ASA intake.It is suggested that acetyl salicylic acid in addition to its inhibitory effect on platelet release reaction, also affects primary aggregation by ADP and possibly interferes with the ability of platelets to activate the contact system of the intrinsic blood coagulation pathway.

Platelet Aggregation in Diabetes Mellitus and the Effect of Insulin in Vivo on Aggregation

1972 ◽  
Vol 27 (01) ◽  
pp. 114-120 ◽  
Author(s):  
A. A Hassanein ◽  
Th. A El-Garf ◽  
Z El-Baz
Keyword(s):  
Platelet Aggregation ◽  
Rapid Onset ◽  
Control Group ◽  
Diabetic Patients ◽  
Fasting State ◽  
Clotting Time ◽  
Cholesterol Levels ◽  
Platelet Disaggregation ◽  
Aggregation And Disaggregation

SummaryADP-induced platelet aggregation and calcium-induced platelet aggregation tests were studied in 14 diabetic patients in the fasting state and half an hour after an intravenous injection of 0.1 unit insulin/kg body weight. Platelet disaggregation was significantly diminished as compared to a normal control group, and their results were negatively correlated with the corresponding serum cholesterol levels. Insulin caused significant diminution in the ADP-induced platelet aggregation as a result of rapid onset of aggregation and disaggregation. There was also a significant increase in platelet disaggregation. In the calcium-induced platelet aggregation test, there was a significant shortening of the aggregation time, its duration, and the clotting time. The optical density fall due to platelet aggregation showed a significant increase. Insulin may have a role in correcting platelet disaggregation possibly through improvement in the intracellular enzymatic activity.

The Effect of Collagen Mediated Platelet Release on Plasma Prekallikrein Activation

1984 ◽  
Vol 51 (01) ◽  
pp. 037-041 ◽  
Author(s):  
K M Weerasinghe ◽  
M F Scully ◽  
V V Kakkar
Keyword(s):  
Platelet Aggregation ◽  
Healthy Volunteers ◽  
Platelet Rich Plasma ◽  
Age Groups ◽  
Inhibitory Effect ◽  
Age Group ◽  
Platelet Factor ◽  
Activated Platelets ◽  
Platelet Release ◽  
Collagen Treatment

SummaryCollagen mediated platelet aggregation caused -5.6 ± 6.7% inhibition and +39.1 ± 15.2% potentiation of prekallikrein activation in plasma from normal healthy volunteers between 20–40 and 50–65 years of age, respectively (n = 15, p <0.01). The amouns of platelet factor-four (PF4) released in the two groups were not significantly different. Collagen treatment in the presence of indomethacin caused +11.5 ± 3.6% and +59.6 ± 19.5% potentiation in the 20–40 and 50–65 age groups respectively (p <0.02). Adrenaline mediated platelet aggregation caused -55.2 ± 7.1% and -35.2 ± 8.3% inhibition in the 20–40 and 50–65 age groups, respectively. Collagen treatment of platelet-deficient-plasma and platelet-rich-plasma in EDTA also caused potentiation of prekallikrein activation.The results indicate that the observed degree of prekallikrein activation after platelet aggregation is a net result of the inhibitory effect of PF4 and the potentiatory effect of activated platelets. The potentiatory effect was greater after collagen treatment as compared to adrenaline treatment, and in the 50–65 age group as compared to the 20–40 age group.

Monitoring of acetyl salicylic acid-induced platelet inhibition with impedance aggregometry in children with systemic-to-pulmonary shunts

2012 ◽  
Vol 23 (2) ◽  
pp. 225-232 ◽  
Author(s):  
Birgitta S. Romlin ◽  
Håkan Wåhlander ◽  
Eva Strömvall-Larsson ◽  
Mats Synnergren ◽  
Fariba Baghaei ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Salicylic Acid ◽  
Platelet Aggregation ◽  
Therapeutic Range ◽  
Platelet Inhibition ◽  
Acetyl Salicylic Acid ◽  
Shunt Thrombosis ◽  
Shunt Implantation ◽  
Paediatric Patients ◽  
Impedance Aggregometry

AbstractBackgroundShunt thrombosis after implantation of systemic-to-pulmonary shunts in paediatric patients is common. Acetyl salicylic acid is used for anti-thrombotic treatment; however, the effect is rarely monitored, although it is known that the response varies. The aim was to determine the effects of acetyl salicylic acid medication on platelet aggregation in children with systemic-to-pulmonary shunts.MethodsA total of 14 children – median age 12 days; ranging from 3 to 100 days – were included in a prospective observational longitudinal study. All children were treated with oral acetyl salicylic acid (3–5 milligrams per kilogram once daily) after shunt implantation. Acetyl salicylic acid-dependent platelet aggregation in whole blood was analysed with impedance aggregometry (Multiplate®) after addition of arachidonic acid. Analyses were carried out before the primary operation, before and 5 and 24 hours after the first acetyl salicylic acid dose, and after 3–6 months of treatment. The therapeutic range for acetyl salicylic acid was defined as a test result less than 60 units.ResultsAcetyl salicylic acid reduced the arachidonic acid-induced platelet aggregation in all but one patient. Of the patients, 93% were in the therapeutic range 5 hours after acetyl salicylic acid intake, 86% were in the range after 24 hours, and 64% after 3–6 months.ConclusionsAcetyl salicylic acid reduces platelet aggregation after shunt implantation in paediatric patients, but a considerable percentage of the children are outside the therapeutic range. Monitoring of platelet aggregation has the potential to improve anti-platelet treatment after shunt implantation by identifying children with impaired acetyl salicylic acid response.

Demonstration of a Plasmatic Cofactor Different from Fibrinogen Necessary for Platelet Release by ADP and Adrenaline

1970 ◽  
Vol 24 (03/04) ◽  
pp. 409-418 ◽  
Author(s):  
S Cronberg ◽  
P Kubisz ◽  
J. P Caen
Keyword(s):  
Salicylic Acid ◽  
Acetyl Salicylic Acid ◽  
Secondary Wave ◽  
Platelet Factor ◽  
Washed Platelet ◽  
Release Reaction ◽  
Platelet Aggregates ◽  
Platelet Release ◽  
Second Wave ◽  
Possible Cause

SummarySecondary wave production and release of platelet factor 4 were studied in washed platelet suspensions and citrate plasma. Induction of a secondary wave requires the presence of large aggregates and a plasmatic cofactor different from fibrinogen. Acetyl-salicylic acid inhibited the production of a second wave both in plasma and platelet suspensions. Plasma taken after the intake of acetyl-salicylic acid induced a second wave in platelets harvested before the intake. The possible production of thrombin or allied enzyme inside the platelet aggregates due to changed internal milieu is suggested as a possible cause of the release reaction induced by ADP and adrenaline. Fundamental differences existed between the release induced by ADP and adrenaline and that induced by collagen, kaolin and other particles.

Inhibition of Thrombin-, Epinephrine- and Collagen-Induced Platelet Aggregation by α1-Acid Glycoprotein

1979 ◽  
Author(s):  
P. Andersen ◽  
C. Eika
Keyword(s):  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Clotting Time ◽  
Acid Glycoprotein ◽  
High Concentrations ◽  
Spontaneous Platelet Aggregation ◽  
Induced Aggregation

α1-Acid glycoprotein (α1,-acid GP) isolated from human plasma was found to inhibit thrombin-induced aggregation of washed human platelets (0.05 NIH U/ml final conc.), and inhibition was complete with physiological concentrations of α1-acid GP (1.0-1.5 g/1 final conc.). The inhibitory effect seemed to occur immediately on thrombin addition, thus similar to the effect of heparin previously observed. As opposed to heparin, however, α1-acid GP did not affect spontaneous platelet aggregation. Furthermore, α1-acid GP (in optimal cone.) reduced the combined inhibitory effect of heparin and antithrombin III on thrombin-induced platelet aggregation, thus consistent with the previous findings using heparin thrombin clotting time.Snyder and Coodley (1976) found α1-acid GP to inhibit platelet aggregation induced by epinephrine and adenosine diphosphate in platelet-rich plasma. As we also found α1-acid GP to inhibit collagen-induced platelet aggregation, α1-acid GP may possibly act as an inhibitor of the release reaction though fairly high concentrations (10 mg/ml final cone.) was needed for complete inhibition.

scholarly journals Inhibitory Effect of Aprotinin on the Activation Process of Contact Factors and Platelet Aggregation

1977 ◽  
Author(s):  
I. Yamaguchi ◽  
Y. Yano ◽  
T. Kitahara ◽  
M. Yatabe ◽  
M. Ukita ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Inhibitory Action ◽  
Enzyme Inhibitor ◽  
Inhibitory Effect ◽  
Release Mechanism ◽  
Activation Process ◽  
Plasma Kallikrein ◽  
Factor Xii ◽  
Clotting Time ◽  
Plasma Factors

It has been reported by several investigators that aprotinin demonstrates inhibitory action on the process of intrinsic blood thromboplastin generation. In this paper the authors will present the facts that on the hydrolytic action of plasma kallikrein, and on the activation process of plasma prekallikrein as well, the inhibitory action of aprotinin is indicated by the use of chromozym PK assay and the latter process might be caused by the inhibition of factor XII activated with Kaolin, and as to platelet aggregation induced by thrombin, aprotinin also plays the inhibitory effect which is more sensitive than the antithrombin activity of aprotinin measured by thrombin clotting time. However, the inhibitory effect of aprotinin on platelets might be caused not only by antithrombic action of this enzyme inhibitor, but also other influence of the inhibitor on release mechanism of the platelets, because epinephrine induced platelet aggregation can be disturbed by the addition of this inhibitor. In summary it mighy be suggested in this study that the clinical use of aprotinin preparation might be one way for anticoagulant thrapy on thrombotic deseases associated with intrinsic hypercoagulability of plasma factors and platelets.

scholarly journals Effect of Mini-Dose of Chlorpromazine on the Bleeding time and Platelet Aggregation

1977 ◽  
Author(s):  
J. Zahavi ◽  
G. Schwartz
Keyword(s):  
Platelet Aggregation ◽  
Bleeding Time ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Serotonin Concentration ◽  
Initial Wave ◽  
Platelet Serotonin ◽  
Significant Prolongation ◽  
Platelet Release

The impairment, of hemostasis by ehlorpromazine (c) at concentrations below those which inhibit platelet release reaction, has been evaluated in 24 normal subjects. In each individual, modidied Ivy bleeding time and platelet aggregations (PAg) induced by adenosine diphosphate (ADP) 0,6 MM and 4 MM collagen 0,003% and 1-epinephrine 3MM well as platelet serotonin concentration, were performed prior to and 20 min. after intramuscular administration of (C) or saline. Normal saline was injected to 6 subjects and 5, 12,5 and 20 mg. of (c) to another 8, 5 and 5 subjects respectively. There was a slight but significant prolongation of the bleeding time and a decrease in the initial wave of aggregation to ADP 0,6 MM in the subjects on (C) compared to those on-saline. Platelet serotonin, however, and (PAg) to collagen, 1-epinephrine and ADP 4 MM, were the same in both groups. The impaired hemostasis by mini-dose of (C) might be attributed to the prevention of leakage of ADP from intact erythrocytes in-vivo and, if so, may signify an important new application of this drug in the treatment of thrombotic disorders.

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