Platelet-activating factor (PAF) receptor antagonists inhibit arachidonic acid induced platelet aggregation in rabbit whole blood

Lipids ◽  
1991 ◽  
Vol 26 (12) ◽  
pp. 1189-1192 ◽  
Author(s):  
Alaina Jean Ammit ◽  
Chris O'Neill
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Whole Blood ◽  
Platelet Activating Factor ◽  
Receptor Antagonists ◽  
Paf Receptor

Inhibition by Glaucocalyxin A of Aggregation of Rabbit Platelets Induced by ADP, Arachidonic Acid and Platelet-Activating Factor, and Inhibition of [3H]-PAF Binding

1992 ◽  
Vol 67 (04) ◽  
pp. 458-460 ◽  
Author(s):  
Zhang Bin ◽  
Long Kun
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Activating Factor ◽  
Northeastern China ◽  
Ethereal Extract ◽  
Ic50 Value ◽  
Rabbit Platelets ◽  
Ic50 Values ◽  
Induced Aggregation

SummaryGlaucocalyxin A is a new diterpenoid isolated from the ethereal extract of the leaves of Rabdosia japonica (Burm f) Hara var glaucocalyx (Maxim) Hara (Labiatae) collected in the northeastern China. When it was incubated with washed rabbit platelets, glaucocalyxin A inhibited ADP- or arachidonic acid-induced platelet aggregation with IC50 values of 4.4 μmol/1, 14.1 μmol/1 respectively. Glaucocalyxin A also inhibited PAF-induced aggregation of rabbit platelets which were refractory to ADP and arachidonic acid with an IC50 value of 13.7 μmol/1. Analysis of [3H]-PAF binding showed that glaucocalyxin A prevented [3H]-PAF binding to intact washed rabbit platelets with an IC50 value of 8.16 μmol/1, which was consistent with its inhibition of PAF-induced platelet aggregation.

scholarly journals Comparison of effect of aloe Vera gel with aspirin and celecoxib on platelet aggregation.

2020 ◽  
Vol 27 (05) ◽  
pp. 973-978
Author(s):  
Sidra Mushtaq ◽  
Zobia Mushtaq ◽  
Javeria Arif ◽  
Mufakhara Fatima ◽  
Sadida Bahawal ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Whole Blood ◽  
Blood Count ◽  
Complete Blood Count ◽  
Platelet Rich Plasma ◽  
Aloe Vera ◽  
Medical Institute ◽  
Aloe Vera Gel ◽  
Study Setting

Objective: This study was designed to compare the effect of Aloe vera gel with aspirin and celecoxib on platelet aggregation. Study Design: Comparative Study. Setting: Post graduate Medical Institute Lahore, Children Hospital, Lahore. Period: September 2015 to September 2016. Material & Methods: Blood was withdrawn from anti-cubital vein, complete blood count was checked, platelet rich plasma was prepared by centrifuging citrated whole blood and then incubated with  Aloe vera low (AVL), Aloe vera high (AVH), aspirin and celecoxib for 30 minutes at 37C. After adding the agonist arachidonic acid, reading was then taken for 3 minutes and percentage aggregation was recorded. Results: Platelet aggregation with aspirin, AVH and AVL was statistically significantly lower as compared to control and celecoxib groups. Conclusion: This study has demonstrateda dose dependentanti-platelet effect of Aloe vera gel which is comparable to aspirin.

scholarly journals Expression of Phosphorylcholine by Histophilus somni Induces BovinePlatelet Aggregation

2006 ◽  
Vol 75 (2) ◽  
pp. 1045-1049 ◽  
Author(s):  
Christopher J. Kuckleburg ◽  
Shaadi F. Elswaifi ◽  
Thomas J. Inzana ◽  
Charles J. Czuprynski
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activating Factor ◽  
Induce Platelet Aggregation ◽  
Histophilus Somni ◽  
Paf Receptor ◽  
Induced Aggregation

ABSTRACT Histophilus somni-induced platelet aggregation was inhibited by antagonists of the platelet-activating factor (PAF) receptor but not inhibitors of PAF synthesis. In addition, H. somni cells expressing phosphorylcholine (ChoP) induced aggregation, while ChoP− H. somni cells did not. This suggests that H. somni ChoP may induce platelet aggregation via interactions with the PAF receptor.

Rapid Assessment of Platelet Function Using Thromboelastography and Small Volumes of Citrated Whole Blood.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3995-3995 ◽  
Author(s):  
Fred G. Pluthero ◽  
Margaret L. Rand ◽  
Victor S. Blanchette ◽  
Walter H. Kahr
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Whole Blood ◽  
Function Analysis ◽  
Maximum Amplitude ◽  
Ease Of Use ◽  
Platelet Response ◽  
Platelet Function Disorders ◽  
Wide Range

Abstract Platelet function disorders are a key cause of abnormal bleeding, and diagnosis is challenging because: platelet abnormalities are diverse, affecting many aspects of function; variability in platelet function testing in clinical laboratories makes it difficult to compare results; large blood volumes required for platelet function analysis make it difficult to perform in neonatal patients; manipulation of platelet rich plasma used for platelet aggregation can lead to test variability; platelet aggregation curves are difficult to interpret in thrombocytopenic patients. We describe a method of testing platelet function using citrated whole blood and thromboelastography (TEG) that overcomes some of these limitations. Commercially-available platelet mapping kits allow the effects of the platelet agonists adenosine diphosphate (ADP) and arachidonic acid (AA) to be assessed via a TEG assay where reptilase and activated factor XIII produce fibrin clots independent of thrombin in heparinized whole blood. The activation and aggregation of platelets is quantified by measuring the difference in maximum amplitude (MA) between unstimulated samples, which form weak fibrin-only clots, and samples with agonists added, which form stronger clots containing fibrin and activated/aggregated platelets. Platelet mapping was used as the basis for a TEG assay which can be used to assess platelet responses to a wide range of stimuli - including ADP, AA, epinephrine, collagen, U46619 (thromboxane-A2 receptor agonist), SFLLRN (PAR-1 thrombin receptor activating peptide) and AYPGKF (PAR-4 activating peptide) - in small samples (330μL) of citrated native (CN) blood or plasma to which heparin is added to a concentration of 20U/mL. Samples were recalcified by adding calcium chloride to 10mM (necessary for the function of reptilase and FXIIIa), and other reagent volumes were the same as in platelet mapping assays, with fibrin activator prepared at 1/2 regular strength. The concentrations of platelet agonists were: collagen 51μg/ml, epinephrine 0.27μM, ADP 5.4μM, arachidonic acid 135μg/mL, U46619 2.6μM, SFLLRN 6.76μM and AYPGKF 34μM. These concentrations produced TEG MA values in heparinated fibrin-activated CN blood from a panel of normal individuals comparable to those obtained from recalcified CN blood in the absence of heparin (the fibrin/platelet response control). The platelet response was rapid with maximum amplitudes reached within 10 minutes for all agonists except collagen, which required >30 minutes to produce maximum amplitude. We have found this TEG platelet-response assay to be useful in detecting platelet function abnormalities, producing results which correlate with and extend those of other platelet function tests. For example in one patient a weak response to epinephrine corresponded to similar platelet aggregation results, and in another the TEG assay detected a weak PAR-1 response not specifically detected in other tests. The assay has also proven useful in assessing platelet function in blood and plasma having low platelet concentrations (<50 x 10E9/L) from experimental or pathological causes (e.g. thrombocytopenia), in titrating platelet responses to agonists and in assessing the effects of antiplatelet agents in vivo and in vitro. Thus this TEG platelet function assay has the advantages of speed, ease of use, flexibility, adaptability to low platelet concentrations and sample economy, requiring small volumes of citrated blood which can be used for other coagulation assays and platelet response tests.

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