scholarly journals The Effect of Imidazole on Human Platelet Aggregation

Blood ◽  
1971 ◽  
Vol 38 (4) ◽  
pp. 417-421 ◽  
Author(s):  
JAMES W. DAVIS ◽  
PHYLLIS E. PHILLIPS
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Glass Bead ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Second Phase ◽  
Platelet Function Tests ◽  
Human Platelet Aggregation ◽  
Function Tests ◽  
Induced Aggregation

Abstract Since imidazole buffers have been used in platelet function tests and the compound has been reported to alter several biochemical activities of platelets, it seemed important to determine whether imidazole influenced platelet aggregation. ADP-induced, collagen-induced, and norepinephrine-induced platelet aggregations were tested in platelet-rich plasma by turbidimetric techniques. Glass bead-induced platelet aggregation in whole blood was tested by a method dependent upon platelet counts. Imidazole, in concentrations of 5mM or less, inhibited aggregation induced by each of these four agents and had negligible effect on the pH of platelet-rich plasma. The second phase of both ADP- and norepinephrine-induced aggregation was inhibited or abolished by imidazole, and 5mM imidazole also inhibited the first phase of norepinephrine-induced aggregation. As little as 0.5 mM imidazole inhibited collagen-induced aggregation in some plasmas. Imidazole appears to be unsuitable for use as a buffer in platelet function tests.

The effects of an ASA-like hydroperoxide compound on adenosine diphosphate induced platelet aggregation

1984 ◽  
Vol 62 (3) ◽  
pp. 338-340
Author(s):  
J. J. F. Killackey ◽  
B. A. Killackey ◽  
I. Cerskus ◽  
R. B. Philp
Keyword(s):  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Pharmacological Property ◽  
Human Platelet ◽  
Adenosine Diphosphate ◽  
Second Phase ◽  
Release Reaction ◽  
Human Platelet Aggregation ◽  
Second Phases ◽  
Induced Aggregation

A hydroperoxide compound structurally related to acetylsalicylic acid, 3-hydroperoxy-3-methylphthalide, inhibits both the first and second phases of adenosine diphosphate induced, biphasic, human platelet aggregation. This occurs over the same concentration range (0.05–0.5 mM) that acetylsalicylic acid inhibits second phase aggregation and the release reaction only. The complete inhibition of adenosine diphosphate induced aggregation is a unique pharmacological property for an acetylsalicylic-acid-like compound.

The Effect of Neuraminidase on Platelet Aggregation Induced by ADP, Norepinephrine, Collagen or Serotonin

1972 ◽  
Vol 28 (02) ◽  
pp. 221-227 ◽  
Author(s):  
James W. Davis ◽  
Kenneth T. N. Yue ◽  
Phyllis E. Phillips
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Second Phase ◽  
Acetylneuraminic Acid ◽  
Negative Surface ◽  
Negative Surface Charge ◽  
Second Phases ◽  
Induced Aggregation

SummaryIncubation of human platelet-rich plasma (PRP) with neuraminidase enhanced platelet aggregation induced by adenosine diphosphate (ADP), norepinephrine, collagen or serotonin. Both first and second phases of ADP- and norepinephrine -induced aggregation were enhanced. In two plasmas a second phase of ADP-induced aggregation occurred after incubation with neuraminidase, but not in the control preparations. In one plasma a second phase of serotonin-induced platelet aggregation occurred after incubation with neuraminidase. The incubation of PRP with exogenous N-acetylneuraminic acid (a product of the action of neuraminidase) had no effect on platelet aggregation. A possible explanation of the observed enhancement of platelet aggregation by neuraminidase is that the enzyme may have released sialic acid from platelet membranes and thereby reduced their net negative surface charge.

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 The Combined Effects of 2,3-Diphosphoglycerate and Phospholipase-A on Platelet Aggregation Induced by ADP, Epinephrine, Norepinephrine and Collagen

1977 ◽  
Author(s):  
M.F. Asterita ◽  
P.G. Iatridis ◽  
S.G. Iatridis ◽  
R. Torrella ◽  
B.H. Ragatz ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Phospholipase A ◽  
Time Dependent ◽  
Second Phase ◽  
Combined Effects ◽  
Dual Channel ◽  
Human Platelet Aggregation ◽  
2,3 Dpg

It has been shown recently, that under specific conditions, phospholipase-A (Phl-A) or 2,3-diphosphoglycerate (2,3-DPG) can inhibit human platelet aggregation induced by ADP, epinephrine, norepinephrine or collagen. In this report, by using a dual channel Payton Aggregometer, the effects of 2,3-DPG and Phl-A on platelet aggregation were further studied. When 2,3-DPG (2μM) was added in human platelet rich plasma with Phl-A (200μU), 30, 60, 120 or 300 sec. before the addition of ADP (0.5-2.0μM), epinephrine (2-5uM) or norepinephrine (2-5μM) an enhancement of platelet aggregation was observed, whereas the same concentration of 2,3-DPG alone or Phl-A alone, inhibited both the rate and extent of the second phase of platelet aggregation induced by the same aggregating substances. The combined effects of 2,3-DPG and Phl-A on collagen induced platelet aggregation remained inhibitory. Aspirin on the other hand abolished the enhancement of platelet aggregation induced by 2,3-DPG and Phl-A. These combined effects of 2,3-DPG and Phl-A were both a concentration and a time dependent response. The results indicate that the combined effects of 2,3-DPG and Phl-A were probably mediated through prostaglandin formation. Since Phl-A is a physiological platelet enzyme which releases arachidonic acid, then we may postulate that 2,3-DPG probably activates the synthetases and/or cyclooxygenases which are the enzymes necessary for the formation of the important platelet aggregating substances, namely the endoperoxides and thromboxanes. Supported by USPHS HL-15425.

Aggregation of Human Platelets by Acidic Mucopolysaccharide Extracted from Stichopus japonicus Selenka

1988 ◽  
Vol 59 (03) ◽  
pp. 435-439 ◽  
Author(s):  
Jia-Zeng Li ◽  
Eric Chun-Yet Lian
Keyword(s):  
Platelet Aggregation ◽  
Sea Cucumber ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Normal Subjects ◽  
Human Platelets ◽  
Second Phase ◽  
Platelet Inhibitors ◽  
Stichopus Japonicus ◽  
Human Platelet Aggregation

SummaryThe acidic mucopolysaccharide extracted from sea cucumber (Stichopus japonicus Selenka) (SJAMP) has been shown to cause platelets to aggregate. Using citrated platelet-rich plasma (PRP), washed platelets and formaldehyde-fixed platelets from humans, we investigated the effects of platelet inhibitors and various plasmas and their fractions on SJAMP-induced platelet aggregation. It was found that the lowest concentration of SJAMP required for the aggregation of human platelets was about 0.4 μg/ ml and the magnitude of aggregation induced by SJAMP was concentration dependent. The platelets were aggregated by SJAMP at 10 μg/ml in 25 out of 28 (89%) normal subjects tested. Platelet inhibitors such as PGE1, aspirin, indomethacin, apyrase, antimycin, 2-deoxy-D-glucose and EDTA inhibited by 70 to 100% the aggregation induced by SJAMP. Washed platelets alone were not aggregated by SJAMP. In the presence of fibrinogetr, washed platelets were aggregated by SJAMP, but formaldehyde-fixed platelets were not. These data indicate that the SJAMP-induced human platelet aggregation requires extracellular calcium, fibrinogen, and energy metabolism. The second phase of aggregation is dependent upon the release of ADP, and cyclooxygenase pathway.

Inhibitory Effect of Staphylokinase on Platelet Aggregation

1993 ◽  
Vol 70 (05) ◽  
pp. 834-837 ◽  
Author(s):  
Akira Suehiro ◽  
Yoshio Oura ◽  
Motoo Ueda ◽  
Eizo Kakishita
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Degradation Products ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Effective Concentration ◽  
Inhibit Platelet Aggregation ◽  
Platelet Suspension ◽  
Washed Platelet ◽  
Human Platelet Aggregation

SummaryWe investigated the effect of staphylokinase (SAK), which has specific thrombolytic properties, on human platelet aggregation. Platelet aggregation induced with collagen was observed following preincubation of platelets in platelet-rich plasma (PRP) or washed platelet suspension (WP) with SAK at 37° C for 30 min. SAK inhibited platelet aggregation in PRP only at the highest examined concentration (1 x 10-4 g/ml). Although SAK did not inhibit platelet aggregation in WP which contained fibrinogen, it did when the platelets had been preincubated with SAK and plasminogen. The most effective concentration in WP was 1 x 10-6 g/ml. The effect could be inhibited by adding aprotinin or α2-antiplasmin. The highest generation of plasmin in the same preincubation fluid was detected at 1 x 10-6 g/ml SAK. We concluded that SAK can inhibit platelet aggregation in WP by generating plasmin and/or fibrinogen degradation products, but is only partially effective in PRP because of the existence of α2-antiplasmin.

Testosterone Potentiation of Ionophore and ADP Induced Platelet Aggregation : Relationship to Arachidonic Acid Metabolism

1981 ◽  
Vol 46 (02) ◽  
pp. 538-542 ◽  
Author(s):  
R Pilo ◽  
D Aharony ◽  
A Raz
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Unsaturated Fatty Acids ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Arachidonic Acid Metabolism ◽  
Ionophore A23187 ◽  
Low Concentrations ◽  
Induced Aggregation

SummaryThe role of arachidonic acid oxygenated products in human platelet aggregation induced by the ionophore A23187 was investigated. The ionophore produced an increased release of both saturated and unsaturated fatty acids and a concomitant increased formation of TxA2 and other arachidonate products. TxA2 (and possibly other cyclo oxygenase products) appears to have a significant role in ionophore-induced aggregation only when low concentrations (<1 μM) of the ionophore are employed.Testosterone added to rat or human platelet-rich plasma (PRP) was shown previously to potentiate platelet aggregation induced by ADP, adrenaline, collagen and arachidonic acid (1, 2). We show that testosterone also potentiates ionophore induced aggregation in washed platelets and in PRP. This potentiation was dose and time dependent and resulted from increased lipolysis and concomitant generation of TxA2 and other prostaglandin products. The testosterone potentiating effect was abolished by preincubation of the platelets with indomethacin.

Enhanced platelet aggregation and activation under conditions of hypothermia

2007 ◽  
Vol 98 (12) ◽  
pp. 1266-1275 ◽  
Author(s):  
Ruben Xavier ◽  
Ann White ◽  
Susan Fox ◽  
Robert Wilcox ◽  
Stan Heptinstall
Keyword(s):  
Cardiac Surgery ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Baseline Levels ◽  
Spontaneous Aggregation ◽  
High Concentrations ◽  
Induced Aggregation ◽  
P2y12 Antagonist

SummaryThe effects on platelet function of temperatures attained during hypothermia used in cardiac surgery are controversial. Here we have performed studies on platelet aggregation in whole blood and platelet-rich plasma after stimulation with a range of concentrations of ADP, TRAP, U46619 and PAF at both 28°C and 37°C. Spontaneous aggregation was also measured after addition of saline alone. In citrated blood, spontaneous aggregation was markedly enhanced at 28°C compared with 37°C. Aggregation induced by ADP was also enhanced. Similar results were obtained in hirudinised blood. There was no spontaneous aggregation in PRP but ADP-induced aggregation was enhanced at 28°C. The P2Y12 antagonist AR-C69931 inhibited all spontaneous aggregation at 28°C and reduced all ADP-induced aggregation responses to small, reversible responses. Aspirin had no effect. Aggregation was also enhanced at 28°C compared with 37°C with low but not high concentrations of TRAP and U46619. PAF-induced aggregation was maximal at all concentrations when measured at 28°C, but reversal of aggregation was seen at 37°C. Baseline levels of platelet CD62P and CD63 were significantly enhanced at 28°C compared with 37°C. Expression was significantly increased at 28°C after stimulation with ADP, PAF and TRAP but not after stimulation with U46619. Overall, our results demonstrate an enhancement of platelet function at 28°C compared with 37°C, particularly in the presence of ADP.

Dependence of Human Platelet Functional Responses on Divalent Cations: Aggregation and Secretion in Heparin- and Hirudin-Anticoagulated Platelet-Rich Plasma and the Effects of Chelating Agents

1981 ◽  
Vol 45 (02) ◽  
pp. 173-179 ◽  
Author(s):  
Bruce Lages ◽  
Harvey J Weiss
Keyword(s):  
Platelet Aggregation ◽  
Chelating Agents ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Divalent Cations ◽  
Normal Subjects ◽  
Concentration Addition ◽  
Functional Responses ◽  
Induced Aggregation

SummaryThe dependence of ADP- and epinephrine-induced platelet aggregation and secretion on extracellular divalent cations was examined by quantitating these responses in citrate-, heparin-, and hirudin-anticoagulated platelet-rich plasma. ADP-induced 14C-5HT secretion in heparin-PRP and hirudin-PRP was generally decreased, relative to that in citrate-PRP, without corresponding reductions in aggregation, whereas in response to epinephrine, both aggregation and secretion were decreased in heparin-PRP, and abolished in hirudin-PRP. In heparin-PRP, but not in hirudin-PRP, the degree to which these responses were altered was highly variable among normal subjects, and was dependent on the anticoagulant concentration. Addition of citrate restored the extent of ADP-induced secretion and of epinephrine-induced aggregation and secretion in heparin-PRP to that observed in citrate-PRP, and increased the extent of ADP-induced secretion in hirudin-PRP. Addition of EDTA or EGTA, however, had no effect on ADP-induced secretion in heparin-PRP. These results suggest that ADP-induced aggregation and secretion, as well as responses to ADP vs. epinephrine, have different dependencies on extracellular or surface-bound divalent cations. The variable responses observed in heparin-PRP may reflect direct interactions of heparin with platelets, and this variability may account for the conflicting results of previous studies.

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