Effects of Acute, Moderate Ethanol Consumption on Human Platelet Aggregation in Platelet-Rich Plasma and Whole Blood

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.

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Endotoxin-Induced Platelet Activation in Human Whole Blood In Vitro

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647499 ◽

1988 ◽

Vol 59 (03) ◽

pp. 378-382 ◽

Cited By ~ 11

Author(s):

Gyorgy Csako ◽

Eva A Suba ◽

Ronald J Elin

Keyword(s):

Platelet Aggregation ◽

Whole Blood ◽

Human Platelet ◽

Platelet Rich Plasma ◽

Atp Release ◽

Human Platelets ◽

Lag Phase ◽

Human Whole Blood ◽

Dose Dependent

SummaryThe effect of purified bacterial endotoxin was studied on human platelets in vitro. In adding up to 1 μg/mL of a highly purified endotoxin, we found neither aggregation nor ATP release in heparinized or citrated human platelet-rich plasma. On the other hand, endotoxin at concentrations as low as a few ng/mL (as may be found in septic patients) caused platelet aggregation in both heparinized and citrated human whole blood, as monitored by change in impedance, free platelet count, and size. Unlike collagen, the platelet aggregation with endotoxin occurred after a long lag phase, developed slowly, and was rarely coupled with measurable release of ATP. The platelet aggregating effect of endotoxin was dose-dependent and modified by exposure of the endotoxin to ionizing radiation. Thus, the activation of human platelets by “solubilized” endotoxin in plasma requires the presence of other blood cells. We propose that the platelet effect is mediated by monocytes and/or neutrophils stimulated by endotoxin.

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Effects of bacterial endotoxin and platelet activating factor (PAF) on human platelet aggregation in native whole blood

Thrombosis Research ◽

10.1016/0049-3848(86)90159-3 ◽

1986 ◽

Vol 44 (5) ◽

pp. 565-573 ◽

Cited By ~ 5

Author(s):

Richard B. Davis ◽

Michelle F. Johnson

Keyword(s):

Platelet Aggregation ◽

Whole Blood ◽

Human Platelet ◽

Platelet Activating Factor ◽

Bacterial Endotoxin ◽

Human Platelet Aggregation

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Human Platelet Aggregation and Release Reaction Induced by Platelet Activating Factor (PAF-Acether) – Effects of Acetylsalicylic Acid and External Ionized Calcium

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661279 ◽

1985 ◽

Vol 53 (02) ◽

pp. 221-224 ◽

Cited By ~ 12

Author(s):

Marco Cattaneo ◽

Maria Teresa Canciani ◽

Pier Mannuccio Mannucci

Keyword(s):

Platelet Aggregation ◽

Acetylsalicylic Acid ◽

Human Platelet ◽

Platelet Rich Plasma ◽

Normal Subjects ◽

Human Platelet Aggregation ◽

Low Concentrations ◽

Before And After ◽

Platelet Secretion

SummaryThe effects of the cyclo-oxygenase inhibition on PAF-acether- induced human platelet aggregation and secretion are controversial. We studied the above parameters on citrated platelet-rich plasma of 12 normal subjects before and after the in vivo administration of acetylsalicylic acid (ASA). Individual sensitivities to PAF-acether were highly variable. ASA completely inhibited the platelet secretion induced by low concentrations of PAF-acether, but caused only partial inhibition when platelets were exposed to high concentrations of PAF-acether. The concentration of PAF-acether which overcame the cyclo-oxygenase inhibition varied substantially, depending on the individual sensitivity of the platelets to it. The addition of CaCl2 2 mM to the samples did not affect the extent of the platelet secretion, but increased irreversible aggregation in samples taken both before and after the ASA administration. These data suggest that low concentrations of PAF-acether stimulate the human platelet secretion by activating the cyclo-oxygenase pathway, whereas higher concentrations also trigger other mechanism(s) that suffice to induce human platelet secretion and full aggregation.

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Inhibitory Effect of Hexahydrocurcumin on Human Platelet Aggregation

Natural Product Communications ◽

10.1177/1934578x1200700719 ◽

2012 ◽

Vol 7 (7) ◽

pp. 1934578X1200700 ◽

Cited By ~ 3

Author(s):

Huei-Ping Dong ◽

Rei-Cheng Yang ◽

I-Chun Chunag ◽

Li-Ju Huang ◽

Hsing-Tan Li ◽

...

Keyword(s):

Platelet Aggregation ◽

Human Platelet ◽

Platelet Rich Plasma ◽

Adenosine Diphosphate ◽

Inhibitory Effect ◽

Human Platelet Aggregation

The effects of hexahydrocurcumin on adenosine diphosphate (ADP)-induced human platelet aggregation were studied. Treatment of human platelet-rich plasma with hexahydrocurcumin resulted in an inhibitory effect on platelet aggregation, suggesting the potential of this compound as an anti-atherosclerogenic agent in humans.

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Estimation of anti-platelet drugs on human platelet aggregation with a novel whole blood aggregometer by a screen filtration pressure method

British Journal of Pharmacology ◽

10.1038/sj.bjp.0704204 ◽

2001 ◽

Vol 133 (8) ◽

pp. 1396-1404 ◽

Cited By ~ 28

Author(s):

Toshiki Sudo ◽

Hideki Ito ◽

Yasushi Ozeki ◽

Yukio Kimura

Keyword(s):

Platelet Aggregation ◽

Whole Blood ◽

Human Platelet ◽

Pressure Method ◽

Filtration Pressure ◽

Human Platelet Aggregation

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Resolvin E1, an EPA-derived mediator in whole blood, selectively counterregulates leukocytes and platelets

Blood ◽

10.1182/blood-2007-11-122598 ◽

2008 ◽

Vol 112 (3) ◽

pp. 848-855 ◽

Cited By ~ 141

Author(s):

Maria Dona ◽

Gabrielle Fredman ◽

Jan M. Schwab ◽

Nan Chiang ◽

Makoto Arita ◽

...

Keyword(s):

Platelet Aggregation ◽

Whole Blood ◽

Human Platelet ◽

Platelet Rich Plasma ◽

Lipid Mediator ◽

Dependent Manner ◽

Omega 3 ◽

Concentration Dependent Manner ◽

Chemokine Production ◽

Thromboxane Receptor

Abstract Resolvin E1 (RvE1) is an omega-3 eicosapentaenoic acid (EPA)–derived lipid mediator generated during resolution of inflammation and in human vasculature via leukocyte-endothelial cell interactions. RvE1 possesses anti-inflammatory and proresolving actions. Here, we report that RvE1 in human whole blood rapidly regulates leukocyte expression of adhesion molecules. RvE1 in the 10- to 100-nM range stimulated L-selectin shedding, while reducing CD18 expression in both neutrophils and monocytes. When added to whole blood, RvE1 did not stimulate reactive oxygen species by either neutrophils or monocytes, nor did it directly stimulate cytokine/chemokine production in heparinized blood. Intravital microscopy (IVM) demonstrated that RvE1 rapidly reduced leukocyte rolling (∼ 40%) in venules of mice. In human platelet-rich plasma (PRP), RvE1 selectively blocked both ADP-stimulated and thromboxane receptor agonist U46619-stimulated platelet aggregation in a concentration-dependent manner. In contrast, Δ6,14-trans-RvE1 isomer was inactive. RvE1 did not block collagen-stimulated aggregation, and regulation of ADP-induced platelet aggregation was not further enhanced with aspirin treatment. These results indicate RvE1 is a potent modulator of leukocytes as well as selective platelet responses in blood and PRP, respectively. Moreover, the results demonstrate novel agonist-specific antiplatelet actions of RvE1 that are potent and may underlie some of the beneficial actions of EPA in humans.

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Simultaneous measurement of adenosine triphosphate release and aggregation potentiates human platelet aggregation responses for some subjects, including persons with Quebec platelet disorder

Thrombosis and Haemostasis ◽

10.1160/th11-10-0740 ◽

2012 ◽

Vol 107 (04) ◽

pp. 726-734 ◽

Cited By ~ 15

Author(s):

Catherine P. M. Hayward ◽

Karen A. Moffat ◽

Jean-Francois Castilloux ◽

Yang Liu ◽

Jodi Seecharan ◽

...

Keyword(s):

Platelet Aggregation ◽

Adenosine Triphosphate ◽

Whole Blood ◽

Human Platelet ◽

Atp Release ◽

Firefly Luciferase ◽

Dense Granule ◽

Human Platelet Aggregation ◽

Platelet Disorder ◽

Platelet Disorders

SummaryPlatelet aggregometry and dense granule adenosine triphosphate (ATP) release assays are helpful to diagnose platelet disorders. Some laboratories simultaneously measure aggregation and ATP release using Chronolume®, a commercial reagent containing D-luciferin, firefly luciferase and magnesium. Chronolume® can potentiate sub-maximal aggregation responses, normalising canine platelet disorder findings. We investigated if Chronolume® potentiates human platelet aggregation responses after observing discrepancies suspicious of potentiation. Among patients simultaneously tested by light transmission aggregometry (LTA) on two instruments, 18/43 (42%), including 14/24 (58%) with platelet disorders, showed full secondary aggregation with one or more agonists only in tests with Chronolume®. As subjects with Quebec platelet disorder (QPD) did not show the expected absent secondary aggregation responses to epinephrine in tests with Chronolu-me®, the reason for the discrepancy was investigated using samples from 10 QPD subjects. Like sub-threshold ADP (0.75 μM), Chronolume® significantly increased QPD LTA responses to epinephrine (p<0.0001) and it increased both initial and secondary aggregation responses, leading to dense granule release. This potentiation was not restricted to QPD and it was mimicked adding 1–2 mM magnesium, but not D-luciferin or firefly luciferase, to LTA assays. Chronolume® potentiated the ADP aggregation responses of QPD subjects with a reduced response. Furthermore, it increased whole blood aggregation responses of healthy control samples to multiple agonists, tested at concentrations used for the diagnosis of platelet disorders (p values <0.05). Laboratories should be aware that measuring ATP release with Chronolume® can potentiate LTA and whole blood aggregation responses, which alters findings for some human platelet disorders, including QPD.

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