scholarly journals Cangrelor (ARC69931MX) produces global inhibition of human platelet function by increasing cAMP levels through a Gi‐independent mechanism.

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Subhashini Srinivasan ◽  
Fozia Mir ◽  
Jin‐Sheng Huang ◽  
Fadi Khasawneh ◽  
Stephen C‐T Lam ◽  
...  
Keyword(s):  
Platelet Function ◽  
Human Platelet ◽  
Independent Mechanism ◽  
Camp Levels ◽  
Global Inhibition

scholarly journals Inhaled NO inhibits platelet aggregation and elevates plasma but not intraplatelet cGMP in healthy human volunteers

2003 ◽  
Vol 285 (2) ◽  
pp. H637-H642 ◽  
Author(s):  
Maurice Beghetti ◽  
Catherine Sparling ◽  
Peter N. Cox ◽  
Derek Stephens ◽  
Ian Adatia
Keyword(s):  
Nitric Oxide ◽  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Human Platelet ◽  
Healthy Human ◽  
Human Volunteers ◽  
Independent Mechanism ◽  
Inhaled No ◽  
Maximal Extent

Effects of inhaled nitric oxide (NO) on human platelet function are controversial. It is uncertain whether intraplatelet cGMP mediates the effect of inhaled NO on platelet function. We investigated the effect of 30 ppm inhaled NO on platelet aggregation and plasma and intraplatelet cGMP in 12 subjects. We performed platelet aggregation studies by using a photooptical aggregometer and five agonists (ADP, collagen, epinephrine, arachidonic acid, and ristocetin). During inhalation, the maximal extent of platelet aggregation decreased by 75% with epinephrine ( P < 0.005), 56% with collagen ( P < 0.005), and 20% with arachidonic acid ( P < 0.05). Responses to ADP (8% P > 0.05) and ristocetin (5% P > 0.05) were unaffected. Platelet aggregation velocity decreased by 64% with collagen ( P < 0.005), 60% with epinephrine ( P < 0.05), 33% with arachidonic acid ( P < 0.05), and 14% with ADP ( P > 0.05). Plasma cGMP levels increased from 2.58 ± 0.43 to 9.99 ± 5.57 pmol/ml ( P < 0.005), intraplatelet cGMP levels were unchanged (means ± SD: 1.96 ± 0.58 vs. 2.71 ± 1.67 pmol/109platelets; P > 0.05). Inhaled NO inhibits platelet aggregation via a cGMP independent mechanism.

Inhibition of human platelet function in vitro and ex vivo by acetaminophen

1989 ◽  
Vol 53 (6) ◽  
pp. 603-613 ◽  
Author(s):  
Bruce Lages ◽  
Harvey J. Weiss
Keyword(s):  
Platelet Function ◽  
Human Platelet ◽  
Ex Vivo

scholarly journals Human platelet microRNA-mRNA networks associated with age and gender revealed by integrated plateletomics

Blood ◽  
2014 ◽  
Vol 123 (16) ◽  
pp. e37-e45 ◽  
Author(s):  
Lukas M. Simon ◽  
Leonard C. Edelstein ◽  
Srikanth Nagalla ◽  
Angela B. Woodley ◽  
Edward S. Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Platelet Function ◽  
Human Platelet ◽  
Web Tool ◽  
Age And Gender ◽  
Key Points ◽  
And Gender ◽  
Unique Dataset

Key Points Unique dataset of human platelet mRNA, miRNA, and physiology reveals mRNAs and miRNAs that differ by age and gender. Interactive public web tool (www.plateletomics.com) provides biologic insights into platelet function and gene expression.

Lack Of Inhibition Of Thromboxane Production Despite Inhibition Of Platelet Function By 1,3-Bis(2 Chloroethyl)-1-Nitrosourea (BCNU)

1981 ◽  
Author(s):  
R McKenna ◽  
T Ahmad ◽  
A Prancan ◽  
D Simon ◽  
H Frischer
Keyword(s):  
Arachidonic Acid ◽  
Oxygen Consumption ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Platelet Function ◽  
Human Platelet ◽  
Thromboxane A2 ◽  
Rabbit Aorta ◽  
Thromboxane Production ◽  
Platelet Thromboxane

We have previously shown that BCNU inhibits human platelet glutathione reductase (GSSG-R) prior to inhibiting platelet function; since thromboxane production is important in platelet function, we evaluated the effect of BCNU induced inhibition of GSSG-R on platelet thromboxane production.Control platelet GSSG-R activity was 0.091 ]jmoles NAD(P)H oxidized min-1lmg-1 protein at 37°C (±0.015 S.D.; n=9); inhibition was detectable at 10-7M% BCNU (70% of control) with a >90% inhibition at and above 10-5M BCNU. Platelet aggregation in response to 1.5×10-3M Arachidonic acid (AA), 10 μM epinephrine, 6 μg/ml equine collagen and 3 μM ADP were inhibited at 10-5M BCNU and abolished at 10-4 BCNU.BCNU (10-3M) did not affect the increase in oxygen consumption induced by AA. Using the rabbit aorta superfusion bioassay for thromboxane A2 (TXA2), threshold concentrations of AA in 10-5 and 10-4 BCNU platelets resulted in an increased measure of aortic tension 13.5 ± 9.4 mm S.D. (n=6) and 23.2 ± 9.5 mm respectively, compared with control values of 4.5 ± 2.4. Acetylsalicylic acid (5 × l0-4M) inhibited the contraction: 1.7 ± 1.1 (n=5). The conversion of 14C AA to thromboxane B2 (TXB2) and PGE2, as measured by radio TLC, was not decreased in BCNU treated platelets. There is a significant increase in TXB2 (p<0.05;n=4) and in the ratio of TXB2:PGE2 in platelets treated with 10-4M BCNU and 10-3M imidazole when compared to platelets treated with imidazole alone.In conclusion BCNU induced inhibition of platelet GSSG-R and platelet function occurs despite preservation of thromboxane production

Prostaglandin E2Differentially Modulates Human Platelet Function through the Prostanoid EP2 and EP3 Receptors

2010 ◽  
Vol 336 (2) ◽  
pp. 391-402 ◽  
Author(s):  
Giovanna Petrucci ◽  
Raimondo De Cristofaro ◽  
Sergio Rutella ◽  
Franco O. Ranelletti ◽  
Davide Pocaterra ◽  
...  
Keyword(s):  
Platelet Function ◽  
Human Platelet

scholarly journals In Vitro Methods to Characterize the Effects of Tobacco and Nontobacco Products on Human Platelet Function

2018 ◽  
Vol 76 (1) ◽  
pp. e46 ◽  
Author(s):  
Shannon G. Loelius ◽  
Sherry L. Spinelli ◽  
Katie L. Lannan ◽  
Richard P. Phipps
Keyword(s):  
Platelet Function ◽  
Human Platelet ◽  
In Vitro Methods

scholarly journals Alteration of Platelet Cyclic AMP (cAMP) by Ethanol

1977 ◽  
Author(s):  
D.H. Cowan ◽  
M. Kikta ◽  
D. Baunach
Keyword(s):  
Cyclic Amp ◽  
Platelet Function ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Platelet Dysfunction ◽  
Camp Metabolism ◽  
Subnormal Level ◽  
Camp Levels ◽  
Stimulation Of

Studies of cAMP in human platelets exposed to ethanol were done to assess one possible mechanism for ethanol-related platelet dysfunction. Ingestion of ethanol by 3 subjects produced blood ethanol levels from 65-76 mM. Thrombocytopenia occurred in 1 subject and impaired platelet function occurred in all. Platelet cAMP decreased 36,51, and 59% below control levels. Infusion of ethanol to 2 normals produced blood ethanol levels of 43 mM and decreased platelet cAMP by 15% and 22%. Incubation of normal platelets with 86 mM ethanol in vitro decreased cAMP from 13.8 ± 2.9 (1 SD) to 9.4 ± 3.5 (p<0.02). By contrast, ethanol did not impair the increase in cAMP that occurred with 1.3 μM PGE1. Further, ethanol enhanced the increase in cAMP produced by 2.0 mM papaverine (Pap) by 160-220% and that produced by Pap + PGE1 by 58%. Dopamine, 0.1 mM, caused a 23% decrease in the basal level of cAMP, a 31% decrease below the subnormal level of cAMP seen with ethanol alone, and a 41% reduction in the increased level of cAMP produced by Pap + ethanol. The effect of ethanol on platelet cAMP metabolism is complex. Ethanol reduces basal levels of cAMP, does not decrease elevated levels that result from PGE1 stimulation of adenylate cyclase, and augments the inhibitory effect of Pap on platelet phosphodiesterase (PDE). Despite causing a decrease in basal cAMP levels, ethanol may impair platelet function by potentiating the effect of agents or other conditions which increase cAMP. The effect of ethanol on Pap-stimulated PDE activity may be blocked by dopamine, a neuropharmacologic agent that is actively accumulated by platelets.

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