Platelet Aggregation Induced by DAS in Vitro: Some Investigations on Its Mechanism of Action

1974 ◽  
Vol 31 (02) ◽  
pp. 354-362
Author(s):  
K. U Benner ◽  
K. A Schumacher ◽  
H. G Classen
Keyword(s):  
Platelet Aggregation ◽  
Mechanism Of Action ◽  
Active Substance ◽  
Platelet Rich Plasma ◽  
The Other ◽  
Second Phase ◽  
Induce Platelet Aggregation ◽  
Release Reaction

SummaryThe effect of the depressor active substance (DAS) on platelets of men, cats, pigs, dogs, rats, and rabbits has been studied by the method of Born (1962). DAS was found to induce platelet aggregation only in human and feline platelet rich plasma (PRP). Nevertheless, there are some striking similarities between platelet aggregation induced by DAS and ADP (i.e. inhibition by the same compounds, such as adenosine, tosylarginine methylester, or p-chloromercuribenzoic acid). The species specifity and a marked tachyphylactic action on platelets of both species makes DAS clearly discernible from all the other aggregation inducing substances which have been studied so far. From additional experiments there is evidence that DAS acts on human and cat platelets via a release reaction of cellular substances known to enhance platelet aggregation in a second phase. This process is strongly dependent on the presence of Ca++.

Enhancement of ADP-induced Platelet Aggregation by Adrenaline in Vivo and Its Prevention

1973 ◽  
Vol 29 (02) ◽  
pp. 490-498 ◽  
Author(s):  
Hiroh Yamazaki ◽  
Itsuro Kobayashi ◽  
Tadahiro Sano ◽  
Takio Shimamoto
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
The Other ◽  
Endothelial Surface ◽  
Important Interaction ◽  
Blood Coagulability ◽  
The Difference

SummaryThe authors previously reported a transient decrease in adhesive platelet count and an enhancement of blood coagulability after administration of a small amount of adrenaline (0.1-1 µg per Kg, i. v.) in man and rabbit. In such circumstances, the sensitivity of platelets to aggregation induced by ADP was studied by an optical density method. Five minutes after i. v. injection of 1 µg per Kg of adrenaline in 10 rabbits, intensity of platelet aggregation increased to 115.1 ± 4.9% (mean ± S. E.) by 10∼5 molar, 121.8 ± 7.8% by 3 × 10-6 molar and 129.4 ± 12.8% of the value before the injection by 10”6 molar ADP. The difference was statistically significant (P<0.01-0.05). The above change was not observed in each group of rabbits injected with saline, 1 µg per Kg of 1-noradrenaline or 0.1 and 10 µg per Kg of adrenaline. Also, it was prevented by oral administration of 10 mg per Kg of phenoxybenzamine or propranolol or aspirin or pyridinolcarbamate 3 hours before the challenge. On the other hand, the enhancement of ADP-induced platelet aggregation was not observed in vitro, when 10-5 or 3 × 10-6 molar and 129.4 ± 12.8% of the value before 10∼6 molar ADP was added to citrated platelet rich plasma (CPRP) of rabbit after incubation at 37°C for 30 second with 0.01, 0.1, 1, 10 or 100 µg per ml of adrenaline or noradrenaline. These results suggest an important interaction between endothelial surface and platelets in connection with the enhancement of ADP-induced platelet aggregation by adrenaline in vivo.

In Vitro and In Vivo Effects of Adrenaline and Phentolamine on Platelet Function

1978 ◽  
Vol 40 (02) ◽  
pp. 428-438 ◽  
Author(s):  
Oreste Ponari ◽  
Emilio Civardi ◽  
Alessandro Megha ◽  
Mario Pini ◽  
Raffaele Poti’ ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Threshold Concentration ◽  
Two Phase ◽  
Platelet Factor ◽  
Induce Platelet Aggregation ◽  
In Vivo Effects ◽  
In Vivo Administration

Summary In vitro and in vivo effects of adrenaline (ADR) on platelet aggregation, on platelet factor 3 (PF3) availability and on platelet factor 4 (PF4) release were studied in man. Inhibitory action of an alpha-blocker, phentolamine (PHEN) was investigated in the same conditions.The threshold concentration (TC) of ADR inducing the typical two-phase response in aggregation tests when added to platelet-rich plasma (PRP) varied in different pools of plasma, but always induced an evident PF4 release and increased PF3 availability. A further increase in both parameters was obtained with higher concentrations but without any significant dose/response correlation.Adding PHEN alone to PRP did not induce platelet aggregation or modify PF4 release induced by stirring, but it reduced PF3 availability. On the other hand, PHEN prevented the effects of ADR in different platelet tests, at appropriate concentrations.Intravenous infusion of ADR lowered the TC, and increased PF3 availability and PF4 release. In vivo administration of PHEN, in contrast, increased TC and reduced PF3 availability, while PF4 remained unchanged.

Studies on the Effect of Platelet Inhibitors on Platelet Adhesion to Collagen and Collagen-Induced Human Platelet Activation

1985 ◽  
Vol 53 (03) ◽  
pp. 337-342 ◽  
Author(s):  
S Krishnamurthi ◽  
V V Kakkar
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Platelet Adhesion ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Antiplatelet Agents ◽  
Calmodulin Antagonist ◽  
Release Reaction ◽  
Low Concentrations

SummaryThe effect of pyridoxal 5’-phosphate (PALP) and trifluoperazine (TFPZ), the calmodulin antagonist, on in vitro platelet adhesion to collagen and collagen-induced platelet activation was studied using platelet-rich-plasma (PRP) or washed platelets (WPL). Platelet aggregation and [14C]-5HT release induced by “threshold” or low concentrations of collagen (0.6 μg/ ml) in PRP were completely abolished by PALP (24 mM), TFPZ (250 μM) as well as indomethacin (10 μM). At higher concentrations of collagen (10–15 μg/ml) in PRP and WPL, the use of stirred and unstirred platelets treated with collagen enabled a distinction to be made between aggregation and adhesion- mediated release reaction. Platelet aggregation and the aggregation-mediated release reaction induced by these concentrations of collagen in stirred platelets were completely abolished by PALP, TFPZ and indomethacin although neither adhesion to collagen nor the adhesion-mediated release reaction of unstirred platelets was significantly affected by these inhibitors. Interestingly, both adhesion and the adhesion-mediated release reaction were abolished by concentrations of PALP 10–40 fold higher than those required to abolish aggregation. Collagen-induced platelet aggregation, but not platelet adhesion, was inhibited in resuspended platelets pretreated with PALP and NaBH4 indicating a separation in the membrane sites involved in aggregation and adhesion. The results further emphasize the distinction between adhesion and aggregation-mediated events with regards to collagen with the latter being more susceptible to inhibition by antiplatelet agents such as PALP and TFPZ.

scholarly journals Effect of anti-P1A1 antibody on human platelets. I. The role of complement

Blood ◽  
1979 ◽  
Vol 53 (4) ◽  
pp. 567-577 ◽  
Author(s):  
DB Cines ◽  
AD Schreiber
Keyword(s):  
Platelet Aggregation ◽  
Complement Activation ◽  
Platelet Rich Plasma ◽  
Plasma Concentrations ◽  
Human Platelets ◽  
Serotonin Release ◽  
Buffer System ◽  
Induce Platelet Aggregation ◽  
Platelet Surface ◽  
Release Reaction

Abstract We studied the interaction of complement with human platelets. Complement was activated by IgG anti-P1A1 antibody obtained from 3 patients with the post-transfusion purpura syndrome. We used a heparin- plasma buffer system that permits complement activation and also preserves platelet function. With this system complement activation was efficient, and platelet immune alteration was extensive. Anti-P1A1 antibody was effective only in the presence of complement, in which case both platelet lysis and serotonin release (release reaction) in the absence of lysis were observed. Platelet lysis, as assessed by 51Cr loss, required 10-fold more antibody than was necessary to induce platelet aggregation and release of 14C-serotonin. This platelet release reaction required an intact classic complement sequence through C6. The extent of platelet serotonin release parallelled the depletion of C1 and C4 from platelet-rich plasma. Concentrations of antibody insufficient to induce platelet aggregation and serotonin release could still activate C1 and deposit increased C3 on the platelet surface. These studies demonstrated that complement activation by anti-P1A1 antibody can alter human platelets in a nonlytic system. Several phases of complement-mediated human platelet alteration are possible, depending on the concentration of anti-P1A1 antibody.

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 Adenosine Diphosphate Induced Aggregation and Release Reaction in Heparinized Platelet Rich Plasma

1977 ◽  
Author(s):  
S. Heptinstall ◽  
G.P. Mulley
Keyword(s):  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Exchange Chromatography ◽  
Second Phase ◽  
Release Reaction ◽  
Ionised Calcium ◽  
Irreversible Aggregation ◽  
Induced Aggregation ◽  
Citrate Release

Preparations of heparinized platelet rich plasma (PRP) from 54 different volunteers were examined to determine the extent of platelet aggregation and release reaction both in the absence and presence of citrate. Platelet aggregation was studied in fresh untreated samples of PRP using a range of concentrations of ADP. To study release reaction platelets in a portion of each preparation were labelled with 3H-5-hydroxytryptamine. Released radioactivity was measured after stirring with ADP or with ADP and citrate.Even in the absence of citrate release was considerable in 26 of the preparations. There was a good correlation between extent of aggregation and extent of release reaction. When second phase aggregation occurred release was extensive, when release was low or absent the higher concentrations of ADP were required to bring about “irreversible” aggregation. Whenever citrate was present release reaction was enhanced. Enhanced release reaction was also observed in PRP in which the bulk of plasma calcium had been exchanged for sodium by ion exchange chromatography.It is concluded that ADP induced release reaction can occur in heparinized PRP but that it is enhanced by reducing the concentration of extracellular ionised calcium.

Evidence for Separate Mechanisms of Induction of the Platelet Release Reaction by Collagen and Adrenaline

1975 ◽  
Author(s):  
O. Tangen ◽  
S. Bygdeman
Keyword(s):  
Platelet Aggregation ◽  
Blood Clotting ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Second Phase ◽  
Release Reaction ◽  
Human Platelet Aggregation ◽  
Small Doses ◽  
Platelet Release ◽  
Induced Aggregation

The effect of some selected inhibitors of platelet release reaction and blood clotting on collagen- and adrenaline-induced human platelet aggregation was investigated by means of the turbidimetric method according to Born. Acetylsalicylic acid (ASA) inhibited both collagen- and adrenaline-induced platelet aggregation in citrated platelet rich plasma (PRP). Addition of sufficient amounts of Ca++ to give concentrations similar to those in native blood suppressed the inhibition by small doses of ASA (5–10 μg/ml) on collagen-induced aggregation and the second phase of adrenaline-induced aggregation. Higher concentrations of ASA (13–30 μg/ml) could partly overcome this effect of Ca++. Heparin, which had no effect on primary adenosine diphosphate (ADP)-induced aggregation, inhibited platelet aggregation induced by collagen. In contrast, both the first and second phase of adrenaline-induced aggregation was markedly potentiated by heparin. Dextran sulphate had effects basically similar to heparin, Nicotinic acid inhibited collagen-induced aggregation, but had no effect on the second phase of adrenaline-induced aggregation. These results indicate that the platelet release reaction induced by collagen and adrenaline is mediated via separate receptors or reaction pathways.

scholarly journals Effect of anti-P1A1 antibody on human platelets. I. The role of complement

Blood ◽  
1979 ◽  
Vol 53 (4) ◽  
pp. 567-577
Author(s):  
DB Cines ◽  
AD Schreiber
Keyword(s):  
Platelet Aggregation ◽  
Complement Activation ◽  
Platelet Rich Plasma ◽  
Plasma Concentrations ◽  
Human Platelets ◽  
Serotonin Release ◽  
Buffer System ◽  
Induce Platelet Aggregation ◽  
Platelet Surface ◽  
Release Reaction

We studied the interaction of complement with human platelets. Complement was activated by IgG anti-P1A1 antibody obtained from 3 patients with the post-transfusion purpura syndrome. We used a heparin- plasma buffer system that permits complement activation and also preserves platelet function. With this system complement activation was efficient, and platelet immune alteration was extensive. Anti-P1A1 antibody was effective only in the presence of complement, in which case both platelet lysis and serotonin release (release reaction) in the absence of lysis were observed. Platelet lysis, as assessed by 51Cr loss, required 10-fold more antibody than was necessary to induce platelet aggregation and release of 14C-serotonin. This platelet release reaction required an intact classic complement sequence through C6. The extent of platelet serotonin release parallelled the depletion of C1 and C4 from platelet-rich plasma. Concentrations of antibody insufficient to induce platelet aggregation and serotonin release could still activate C1 and deposit increased C3 on the platelet surface. These studies demonstrated that complement activation by anti-P1A1 antibody can alter human platelets in a nonlytic system. Several phases of complement-mediated human platelet alteration are possible, depending on the concentration of anti-P1A1 antibody.

Blood Platelet Behaviour in Mothers and Neonates

1985 ◽  
Vol 53 (03) ◽  
pp. 428-432 ◽  
Author(s):  
N P Andrews ◽  
F Broughton Pipkin ◽  
S Heptinstall
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Blood Platelet ◽  
Inhibitory Effects ◽  
Induce Platelet Aggregation ◽  
Release Reaction

SummaryBlood platelet behaviour was compared in mothers at birth and their babies, and in non-pregant, female controls. Platelet responses to arachidonic acid (AA) and to adrenaline were measured in platelet-rich plasma and the inhibitory effects of prostacyclin (PGI2) were determined. Platelets from the mothers differed from those from the neonates and controls in that lower concentrations of AA were needed to induce platelet aggregation and a release reaction. In addition, more PGI2 was needed to inhibit AA-induced platelet aggregation. Platelets from the neonates differed from the mothers and controls in that they were almost completely insensitive to adrenaline. They did not differ from the controls in their sensitivity to AA or PGI2 but the extent of the release reaction induced by AA was significantly reduced.

scholarly journals Therapeutic Ultrasound - An Inducer of Platelet Aggregation in Vitro

1977 ◽  
Author(s):  
B.V. Chater ◽  
A.R. Williams ◽  
J.H. Sanderson
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Therapeutic Ultrasound ◽  
Red Cells ◽  
Platelet Destruction ◽  
Release Reaction ◽  
Plasma Haemoglobin ◽  
Lower Frequencies

Exposure of human platelet rich plasma to therapeutic levels of ultrasound, was found to initiate platelet aggregation and release in vitro. The amount of aggregation, as assessed using a modified platelet aggregometer was found to be related to both the intensity and frequency of the ultrasound. Aggregation occurred at a faster rate and was more extensive at lower frequencies (0.75MHz) and higher intensities. The ability to induce aggregation was found to be directly related to platelet sensitivity to ADP, more sensitive platelets responding to lower intensities of ultrasound. Experiments monitoring the release of 3 thromboglobulin, a marker of the release reaction, indicated that ultrasound was inducing release in two distinct ways.Firstly by the physical disruption of a number of platelets, and secondly by ADP released from the disrupted platelets inducing further release. Release and platelet aggregation was found to parallel the disruption of red cells, as measured by plasma, haemoglobin levels, and this coupled with the greater effect at lower frequencies is thought to indicate that platelet destruction is occurring by cavitation.

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