scholarly journals Interaction of a chick skin collagen fragment (alpha1-CB5) with human platelets. Biochemical studies during the aggregation and release reaction.

1975 ◽  
Vol 250 (17) ◽  
pp. 6916-6922 ◽  
Author(s):  
T M Chiang ◽  
E H Beachey ◽  
A H Kang
Keyword(s):  
Human Platelets ◽  
Release Reaction ◽  
Skin Collagen ◽  
Biochemical Studies ◽  
Collagen Fragment

Release, Aggregation and Lysis of Human Platelets by Antilymphocyte Globulin and Antiplatelet Serum

1976 ◽  
Vol 36 (02) ◽  
pp. 411-423 ◽  
Author(s):  
Nicholas Lekas ◽  
J. C Rosenberg
Keyword(s):  
Platelet Aggregation ◽  
Gamma Globulin ◽  
Human Platelets ◽  
Plasma Medium ◽  
Release Reaction ◽  
Clinical Events ◽  
Thrombotic Complications ◽  
Platelet Release ◽  
Free Media

SummaryHuman platelets labeled with 51Cr were used to determine the contribution made by platelet lysis to the platelet release reaction and platelet aggregation induced by rabbit antihuman platelet serum (APS) and equine antihuman thymocyte globulin (ATG). Platelets were tested in both plasma (PRP) and non-plasma containing media. Antibodies directed against platelets, either as APS or ATG, induced significant amounts of platelet release and aggregation, as well as some degree of lysis, in the absence of complement. The presence of complement increased platelet lysis and aggregation, but not the release reaction. Non-immune horse gamma globulin produced different responses depending upon whether platelets were investigated in PRP or non-plasma containing media. Aggregation was seen in the latter but not the former. These differences can be explained by the presence of plasma components which prevent non-specific immune complexes from causing platelet aggregation. Since platelets in vivo are always in a plasma medium, one must be wary of utilizing data from platelet studies in synthetic plasma-free media as the basis of explaining clinical events. These observations demonstrate at least two, and possibly three, different mechanisms whereby ATG could activate platelets causing thrombotic complications and thrombocytopenia, i.e., via 1) specific and, 2) non-specific non-lytic pathways and 3) a lytic pathway.

The paradox of tianeptine

1993 ◽  
Vol 8 (S2) ◽  
pp. 89s-93s ◽  
Author(s):  
M Ansseau
Keyword(s):  
Chronic Conditions ◽  
Depressive Disorders ◽  
Antidepressant Activity ◽  
Synaptic Cleft ◽  
Human Platelets ◽  
Mechanisms Of Action ◽  
Functional Deficit ◽  
Number Of Patients ◽  
Biochemical Studies ◽  
Antidepressant Efficacy

SummaryThe classical biochemical hypothesis of depression posits a functional deficit in central neurotransmitter systems, particularly serotonin (5-HT) and/or noradrenaline. The major support for this theory was that antidepressants increase the amount of neurotransmitters in the synaptic cleft, by inhibiting reuptake mechanisms (tricyclics) or inhibiting enzymatic catabolism (MAOIs). The major role suggested for 5-HT in this theory led to the development of a large number of compounds which selectively inhibit 5-HT reuptake, such as fluvoxamine, fluoxetine, citalopram, sertraline, paroxetine, etc. Numerous clinical studies have demonstrated the antidepressant activity of such types of agents, supporting 5-HT deficit as the main origin of depression. Tianeptine is active in classical animal models of antidepressants. Its antidepressant efficacy has been established in controlled trials involving a large number of patients. Several biochemical studies however demonstrated that tianeptine induces in acute as well as in chronic conditions, a presynaptic increase of 5-HT reuptake, both in animal and human platelets and animal CNS. Therefore, as a 5-HT reuptake enhancer, tianeptine exhibits a mechanism of action totally opposite to 5-HT reuptake blockers such as fluoxetine but, paradoxically, both mechanisms of action are associated with a therapeutic activity in depressive disorders. Several hypotheses to explain these paradoxical findings and different methodologies to test them clinically are proposed.

scholarly journals Survival and recovery of human platelets stored for five days in a non- plasma medium

Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 672-675 ◽  
Author(s):  
GA Adams ◽  
SD Swenson ◽  
G Rock
Keyword(s):  
Platelet Aggregation ◽  
Human Blood ◽  
Blood Platelets ◽  
Human Platelets ◽  
Plasma Medium ◽  
Release Reaction ◽  
In Vivo Recovery ◽  
Human Blood Platelets

Abstract Human blood platelets were stored for five days as concentrates in 60 mL of: (a) plasma; (b) non-plasma medium with anticoagulant; and (c) non-plasma medium without anticoagulant. All preparations were equally functional when tested for platelet aggregation and release reaction in response to single agonist or synergistic pairs of agonists in vitro. Platelets stored in non-plasma medium with anti-coagulant had lower kallikrein, fibrino(gen)peptide A, lactate, and beta-thromboglobulin than did plasma controls after five days. In vivo recovery and survival of platelets stored in non-plasma medium with anticoagulant were 51.2% +/- 4.3% and 8.7 +/- 0.3 days, respectively, which were not statistically different from plasma controls of 39.2% +/- 4.9% and 7.2 +/- 0.8 days, respectively. It is concluded that platelets can be stored for five days in a non-plasma medium and still have good in vivo recoveries and survivals.

The Role Of Glycoprotein V (GPV) In Thrombin Activation Of Human Platelets

1981 ◽  
Author(s):  
K Fujimura ◽  
S Maehama ◽  
A Kuramoto
Keyword(s):  
Membrane Surface ◽  
Human Platelets ◽  
Surface Proteins ◽  
Galactose Oxidase ◽  
Membrane Glycoproteins ◽  
Release Reaction ◽  
Sds Page ◽  
Thrombin Activation ◽  
Platelet Release

The analysis of platelet membrane glycoproteins and platelet functions was conducted to disclose the role of GPI and V in the thrombin activation of platelet. Our previous study proved that native and HNB thrombin hydrolyzed GPV(M. W.8-9 × 104) selectively and released new glycoprotein fragment (M.W. 6.2-6.8 × 104 ) of GPV, resulting in the development of 14C-5HT release reaction and platelet MDA production. But DIP thrombin could not induce these phenomena.Membrane surface proteins of intact platelets were labeled with Na[3H]BH4 by neuraminidase and galactose oxidase method and analyzed by fluorography after SDS-PAGE.The high molecular weight glycoproteins, GPI, GPIII and GPV were diminished by trypsin treatment in correlation with the concentration and incubation time. In correspond to the diminution of these membrane glycoproteins, platelet release reaction was increased .Chymotrypsin treatment in various concentrations, release reaction and MDA production were not induced in spite of long incubation times. But the ristocetin aggregation was decreased in Chymotrypsin treated platelets whose membrane glycoproteins did not change significantly. The Chymotrypsin treated platelets whose GPI was modified functionally, showed normal release reaction and MDA production by thrombin stimulation. On the other hand, the thrombin treated platelets in low concentration previously whose GPV was hydrolyzed partially, demonstrated little release reaction and MDA production by thrombin or trypsin stimulation. From these results, the GPV was hydrolyzed specifically by thrombin and nonspecifically by trypsin but was not hydrolyzed by Chymotrypsin. It was concluded that the thrombin binds to the GPI and hydrolyzed GPV specifically, and hydrolysis of GPV might act as a signal to induce the platelet release reaction and prostaglandin metabolism.

Factors Influencing Thrombin Induced Platelet Release Reaction

1979 ◽  
Author(s):  
E. Hattey ◽  
B.R. Binder
Keyword(s):  
Platelet Count ◽  
Human Platelets ◽  
Serotonin Release ◽  
Major Influence ◽  
Release Reaction ◽  
Platelet Counts ◽  
Ph Values ◽  
Factors Influencing ◽  
Platelet Release ◽  
Phosphate Buffered Saline

To study the effect of pH and platelet counts on thrombin induced platelet release reaction, washed human platelets labeled with 14C-serotonin were suspended in phosphate buffered saline of varying pH values for 15 minutes with thrombin concentrations between 1,1 and 0,068 NIH U/ml of suspension. The amount of serotonin released caused by the thrombin added was dependent on the pH of the incubation medium with an optimum in the range of pH 7,4 -7,6. This effect was more marked with higher thrombin concentrations. The serotonin release controles without thrombin were not influenced by the different pH values and were always less than 10%. The amount of platelets in the reaction mixture influenced the release values not significantly at thrombin concentrations of 1,1 and 0,27 NIH U/ml While with 0,068 NIH U/ml a significant dependence of the release on the number of platelets was observed, resulting in higher release values in platelet mixtures with lower platelet counts.Therefore it can be concluded that the pH is of major influence on the release reaction especially at high thrombin concentrations while the platelet count is of importance only at low thrombin concentrations.

scholarly journals Effect of anti-P1A1 antibody on human platelets. II. Mechanism of the complement-dependent release reaction

Blood ◽  
1979 ◽  
Vol 53 (4) ◽  
pp. 578-587 ◽  
Author(s):  
AD Schreiber ◽  
DB Cines ◽  
C Zmijewski ◽  
RW Colman
Keyword(s):  
Human Platelets ◽  
Metabolic Energy ◽  
Igg Antibody ◽  
Platelet Surface ◽  
Release Reaction ◽  
Platelet Release ◽  
High Concentrations ◽  
Antibody Levels ◽  
Pharmacologic Agents

Abstract We studied the mechanism by which complement activated by anti-P1A1 antibody elicits the platelet release reaction. Anti-P1A1 antibody mediates its action through the classic complement pathway, and its effect depends on the concentration of IgG antibody on the platelet surface. At relatively high concentrations of anti-P1A1 antibody the release reaction was mediated by a mechanism in part independent of extracellular ADP and metabolic energy and inhibited by only high concentrations of PGE1. However, at lower concentrations of anti-P1A1 antibody the release reaction was dependent on metabolic energy and ADP, and the concentration of PGE1 required to inhibit platelet release was similar to that required to inhibit ADP-induced release. The cyclooxygenase inhibitor acetylsalicylic acid inhibited the release reaction at all nonlytic antibody levels studied. None of the agents studied inhibited the induction of platelet lysis by very high concentrations of anti-P1A1 antibody, and no effect of antibody on platelet 14C-serotonin uptake was observed at antibody concentrations that did not mediate direct in vitro alteration. These studies suggest the possible use of pharmacologic agents in modifying some complement- mediated platelet alterations.

Platelet sialic acid and platelet survival after aggregation by ADP

Blood ◽  
1980 ◽  
Vol 56 (5) ◽  
pp. 876-880
Author(s):  
MA Packham ◽  
MA Guccione ◽  
RL Kinlough-Rathbone ◽  
JF Mustard
Keyword(s):  
Sialic Acid ◽  
Human Platelets ◽  
Platelet Surface ◽  
Release Reaction ◽  
Dense Granules ◽  
Total Sialic Acid ◽  
Platelet Survival ◽  
Rabbit Platelets ◽  
Induced Aggregation

Some investigators have reported recently that platelet surface sialic acid is decreased during ADP-induced aggregation, whereas others have reported an increase. Since removal of sialic acid from the platelet surface shortens platelet survival, we have determined the survival of platelets that have been aggregatad by ADP. We have also measured the amount of sialic acid in the suspending fluid of platelets after ADP- induced aggregation. ADP-induced aggregation did not cause the loss of sialic acid from rabbit platelets (which do not undergo a release reaction in response to ADP) nor from washed human platelets in a medium containing physiologic concentrations of calcium in which granule contents are not released. In a medium without added calcium, ADP caused the release of 14C-serotonin (42.5% +/- 3%) from human platelets, but less than 4% of the sialic-acid-containing material was released. It seems likely that little of the releasable sialic acid of platelets is in the dense granules or the alpha-granules. Thrombin (5 U/ml) released 90.0% +/- 3.4% of the serotonin from human platelets but only 20.6% +/- 7.4% of the total sialic-acid-containing material. Neuraminidase removed 42.3% of the total sialic acid, presumably from the platelet surface. Rabbit platelets that had been aggregated by ADP and deaggregated survived normally when returned to the circulation. This observation also provides evidence that they had not lost membrane sialic acid during aggregation and deaggregation.

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