A NOVEL APPROACH TO INHIBIT THE ANTICOAGULANT-INDUCED SPONTANEOUS ACTIVATION OF BLOOD PLATELETS - EFFECT OF MAGNESIUM ON PLATELET RELEASE REACTION IN WHOLE BLOOD

1997 ◽  
Vol 85 (2) ◽  
pp. 127-132 ◽  
Author(s):  
Jacek Golański ◽  
Tadeusz Pietrucha ◽  
Zbigniew Baj ◽  
Janusz Greger ◽  
Cezary Watala
Keyword(s):  
Whole Blood ◽  
Blood Platelets ◽  
Release Reaction ◽  
Novel Approach ◽  
Platelet Release ◽  
Spontaneous Activation

Enhancement of the Release Reaction Not Accompanied with Enhanced Phosphatidylinositol Turnover in the Reserpinized Rabbit Blood Platelets

1983 ◽  
Vol 50 (02) ◽  
pp. 595-600 ◽  
Author(s):  
Y Watanabe ◽  
M Soda ◽  
N Fukamachi ◽  
B Kobayashi
Keyword(s):  
Phosphatidic Acid ◽  
Blood Platelets ◽  
Specific Protein ◽  
The Other ◽  
Release Reaction ◽  
Rabbit Blood ◽  
Phosphatidylinositol Turnover ◽  
Activated State ◽  
32P Incorporation ◽  
Platelet Release

SummaryThrombin-induced platelet release reaction examined with secretion of calcium and N-acetylglucosaminidase was significantly enhanced in the platelets from reserpine-treated rabbits as compared with the control. On the other hand, 32P-incorporation into phosphatidic acid was suppressed in the reserpinized platelets in activated state. Thrombin induced phosphatidylinositol (PI)- breakdown, which was examined by decreases in radioactivity and content of PI, and an increase in diacylglycerol, was not enhanced in the reserpinized platelets as compared with the control. The phosphorylation of the specific protein coupled to thrombin- induced platelet PI-breakdown was not stimulated in the reserpinized platelets as compared with the control. In contrast to PI, PC-degradation by thrombin was significantly stimulated in the reserpinized platelets. Possible existence of pathway(s) other than that associated with an enhancement of Pl-tumover is conceivable as a mechanism involved in platelet release reaction.

Platelet release reaction in whole blood

1983 ◽  
Vol 31 (5) ◽  
pp. 759-763
Author(s):  
M.A. Schattner ◽  
M.A. Lazzari
Keyword(s):  
Whole Blood ◽  
Release Reaction ◽  
Platelet Release

Liquid chromatography of serotonin and adenine nucleotides in blood platelets, illustrated by evaluation of functional integrity of platelet preparations.

1985 ◽  
Vol 31 (5) ◽  
pp. 695-698 ◽  
Author(s):  
O C Ingebretsen ◽  
A M Bakken ◽  
M Farstad
Keyword(s):  
Adenine Nucleotides ◽  
Blood Platelets ◽  
Energy Charge ◽  
Adenylate Energy Charge ◽  
Experimental Procedure ◽  
Release Reaction ◽  
Functional Integrity ◽  
Chromatographic Procedure ◽  
Platelet Release ◽  
Liquid Chromatographic

Abstract In this relatively rapid liquid-chromatographic procedure the endogenous serotonin in blood platelets is quantified by fluorometry. We used this experimental procedure to estimate the platelet-release reaction as an indicator of the functional integrity of stored platelets. a decrease in the platelet-release reaction more sensitively indicates platelet changes during storage than do alterations in total ATP concentration or adenylate energy charge. The described method for quantifying serotonin is convenient enough for routine use in blood banks.

The Potentiation of Platelet Aggregation and Adhesion by Heparin in Vitro and in Vivo

1973 ◽  
Vol 45 (4) ◽  
pp. 485-494 ◽  
Author(s):  
C. Thomson ◽  
C. D. Forbes ◽  
C. R. M. Prentice
Keyword(s):  
Platelet Aggregation ◽  
Intravenous Injection ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Test Cell ◽  
Release Reaction ◽  
Platelet Release ◽  
Increase Platelet Aggregation

1. Heparin has been shown to increase platelet aggregation by ADP and adrenaline and to enhance the platelet release reaction when tested in citrated platelet-rich plasma (P.R.P.). This activity is present when heparin is added to P.R.P. or when P.R.P. is prepared after intravenous injection of heparin, and when heparin is added to non-anticoagulated native P.R.P. 2. Retention of platelets by cellophane membranes within a specially designed test-cell was significantly increased when heparin was added to citrated whole blood. 3. Though aspirin blocks the release reaction with and without heparin, it does not prevent the potentiation of initial ADP or first wave adrenaline aggregation caused by heparin.

scholarly journals Effects of collagen and of aspirin on the concentration of guanosine 3′:5′-cyclic monophosphate in human blood platelets: measurement by a prelabelling technique (Short Communication)

1974 ◽  
Vol 138 (2) ◽  
pp. 317-320 ◽  
Author(s):  
R. J. Haslam ◽  
M. D. McClenaghan
Keyword(s):  
Human Blood ◽  
Cyclic Gmp ◽  
Short Communication ◽  
Blood Platelets ◽  
Release Reaction ◽  
Cyclic Monophosphate ◽  
Platelet Release ◽  
Human Blood Platelets

A method is described for isolating cyclic [3H]GMP from platelets preincubated with [3H]guanine. Collagen increased and aspirin decreased the cyclic [3H]GMP concentration in platelets. The results are consistent with a role for cyclic GMP in the platelet release reaction.

3-D organization of fibrinogen receptors using computer reconstruction and whole-mount microscopy

1988 ◽  
Vol 46 ◽  
pp. 30-31
Author(s):  
E. T. O'Toole ◽  
R. R. Hantgan ◽  
J. C. Lewis
Keyword(s):  
Whole Blood ◽  
Colloidal Gold ◽  
Blood Platelets ◽  
Cell Contact ◽  
Computer Assisted ◽  
Adherent Cells ◽  
Differential Centrifugation ◽  
Computer Reconstruction ◽  
Sds Page ◽  
Whole Mount

Thrombocytes (TC), the avian equivalent of blood platelets, support hemostasis by aggregating at sites of injury. Studies in our lab suggested that fibrinogen (fib) is a requisite cofactor for TC aggregation but operates by an undefined mechanism. To study the interaction of fib with TC and to identify fib receptors on cells, fib was purified from pigeon plasma, conjugated to colloidal gold and used both to facilitate aggregation and as a receptor probe. Described is the application of computer assisted reconstruction and stereo whole mount microscopy to visualize the 3-D organization of fib receptors at sites of cell contact in TC aggregates and on adherent cells.Pigeon TC were obtained from citrated whole blood by differential centrifugation, washed with Ca++ free Hank's balanced salts containing 0.3% EDTA (pH 6.5) and resuspended in Ca++ free Hank's. Pigeon fib was isolated by precipitation with PEG-1000 and the purity assessed by SDS-PAGE. Fib was conjugated to 25nm colloidal gold by vortexing and the conjugates used as the ligand to identify fib receptors.

On the Mechanism by which Cell Contact Induces the Release Reaction of Blood Platelets; the Effect of Cationic Polymers

1972 ◽  
Vol 27 (01) ◽  
pp. 121-133 ◽  
Author(s):  
P Massini ◽  
E. F Lüscher
Keyword(s):  
Human Blood ◽  
Calcium Ions ◽  
Blood Platelets ◽  
Cell Contact ◽  
Second Phase ◽  
Cationic Polymers ◽  
Release Reaction ◽  
Per Se ◽  
Human Blood Platelets

SummaryHuman blood platelets are aggregated by the basic polymers polylysine and DEAE- dextran. Under certain conditions a second phase of aggregation, concomitant with the release reaction, is elicited. The presence of ADP, calcium ions and a plasmatic cofactor within the primary aggregates are necessary for the induction of the release reaction. These experiments demonstrate that cell contact per se does not lead to a release reaction ; in order to become effective it must take place in the presence of ADP.

Effect of Aspirin on the Thrombelastogram of Human Blood

1973 ◽  
Vol 30 (03) ◽  
pp. 494-498 ◽  
Author(s):  
G de Gaetano ◽  
J Vermylen
Keyword(s):  
Oral Dose ◽  
Single Oral Dose ◽  
Platelet Function ◽  
Human Blood ◽  
Platelet Rich Plasma ◽  
Plasma Samples ◽  
Release Reaction ◽  
Platelet Release

SummaryThrombelastograms of both native blood and re-calcified platelet-rich plasma samples taken from subjects given a single oral dose of aspirin (1 gram) were not significantly different from the pretreatment recordings. Aspirin also did not modify the thrombelastogram when preincubated in vitro with platelet-rich plasma at concentrations inhibiting the platelet “release reaction” by collagen. Thrombelastography therefore cannot evaluate the effect of aspirin on platelet function.

The Effect of the Phospholipase Inhibitor Mepacrine on Platelet Aggregation, the Platelet Release Reaction and Fibrinogen Binding to the Platelet Surface

1981 ◽  
Vol 45 (03) ◽  
pp. 257-262 ◽  
Author(s):  
P D Winocour ◽  
R L Kinlough-Rathbone ◽  
J F Mustard
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Surface ◽  
Release Reaction ◽  
Fibrinogen Binding ◽  
Platelet Release

SummaryWe have examined whether inhibition by mepacrine of freeing of arachidonic acid from platelet phospholipids inhibits platelet aggregation to collagen, thrombin or ADP, and the release reaction induced by thrombin or collagen. Loss of arachidonic acid was monitored by measuring the amount of 14 C freed from platelets prelabelled with 14 C-arachidonic acid. Mepacrine inhibited 14 C loss by more than 80% but did not inhibit thrombin-induced platelet aggregation and had a small effect on release. ADP-induced platelet aggregation did not cause 14 C loss. Mepacrine inhibited ADP-induced platelet aggregation by inhibiting the association of fibrinogen with platelets during aggregation. The effect of mepacrine on fibrinogen binding could be considerably decreased by washing the platelets but the inhibition of 14 C loss persisted. Platelets pretreated with mepacrine and then washed show restoration of aggregation to collagen. Thus, mepacrine has two effects; 1. it inhibits phospholipases, 2. it inhibits fibrinogen binding. Freeing of arachidonic acid is not necessary for platelet aggregation or the release reaction.

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