The Effects Of Chemical Alterations Of The Benzoic Acid Nucleus On Platelet Function And Prostacyclin Activity In The Arterial Wall

1981 ◽  
Author(s):  
B A Killackey ◽  
J J Killackey ◽  
R B Philp
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Benzoic Acid ◽  
Platelet Function ◽  
Platelet Rich Plasma ◽  
Atp Release ◽  
Rabbit Aorta ◽  
Arachidonic Acid Metabolism ◽  
Second Phase ◽  
Benzoic Acid Derivatives

The effects of a series of benzoic acid derivatives (ASA analogs) on prostacyclin (PGI2) synthesis by rabbit aorta rings and on human platelet function were examined to determine if antiplatelet activity could be separated from anti-PGI2 activity.Rings of rabbit aorta were incubated with or without drugs in Tris 0.05 M, pH 7.5 for 6 m at room temperature (R.T.). Supernatant was then transferred to platelet-rich plasma incubated at 37°C for 3 m. ADP was added 60 s later and aggregation was measured and compared to controls. Rings were also incubated with 14C-arachidonic acid (14C-AA) for 60 m at R.T. in Tris with or without drugs. Products were extracted and measured by radio-T.L.C. along with known standards. Platelet aggregation and release of ATP were measured using a ChronoLog Lumi aggregometer. The effects of these agents on PGI2 activity were similar to their effects on platelet aggregation. ASA however did not exhibit the marked inhibitory potency that it had on the second phase of platelet aggregation and ATP release. Changing the 2-acetoxy group of A.S.A. to a 2-acetyl or 3-propionyloxy resulted in a loss of inhibitory activity in both systems. 2-Propionyloxy substitution resulted in a similar spectrum of activity to ASA. The effects of these agents on the metabolism of 14C-AA by rabbit aorta rings generally confirmed the bioassay results although some of the agents had novel effects on blood vessel arachidonic acid metabolism.Despite potential species differences, this study demonstrates an inability to separate antiplatelet and anti-PGI2 effects with this series of benzoic acid derivatives. Further study of the effects of these agents on the metabolism of 14C-AA by rings of rabbit aorta may lead to a better understanding of PGI2 formation.

Pioglitazone Inhibits Platelet Function and Potentiates the Effects of Aspirin

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1228-1228
Author(s):  
John P. Mongan ◽  
Hanna Mieszczanska ◽  
Richard P. Phipps ◽  
Charles W. Francis
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Blood Sample ◽  
Platelet Function ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Platelet Rich Plasma ◽  
Atp Release ◽  
Thromboxane B2 ◽  
Pparγ Agonists

Abstract Abstract 1228 BACKGROUND: Thiazolidinediones (TZDs) are agonists of PPARγ which favorably modify metabolic parameters and markers of atherosclerosis among type 2 diabetics. Enucleate platelets express PPARγ protein, and PPARγ agonists blunt release of CD40L and thromboxane B2 (TXB2) from thrombin-activated platelets. (Abbiyik, F et al, Human bone marrow megakaryocytes and platelets express PPARγ and PPARγ agonists blunt platelet release of CD40 ligand and thromboxanes. Blood, 2004 104(5):p.1361–8.) Diabetic subjects disproportionately experience arterial thromboses despite aspirin therapy. We assessed platelet function after pioglitazone in two risk groups in the presence and absence of aspirin to characterize its range of antiplatelet effect. SUBJECTS: 20 diabetic and 20 non-diabetic subjects were enrolled in a prospective study. Exclusion criteria among all subjects included current use of antiplatelet, anticoagulants, or pioglitazone, bleeding disorder, renal or liver disease, congestive heart failure, pregnancy or hypersensitivity to aspirin or pioglitazone. Non-diabetic subjects were excluded for BMI > 30 kg/m2, cardiovascular disease or risk factors. All subjects previously on aspirin underwent a 7 day minimum “wash-out” period. METHODS: Four separate blood samples from each subject were collected on 2 separate days separated by a 7 day interval. On day 1, a baseline blood sample was obtained followed by a second blood sample 3 hours after ingestion of 30 mg pioglitazone. Subjects returned 1 week later after having taken a single 81 mg aspirin 2–3 hours before arrival. Samples 3 and 4 were collected in the same manner as during week 1. Platelet rich plasma (PRP) was immediately prepared and platelet aggregation performed by the turbidometric method of Born with simultaneous measurement of ATP release. ADP (5M and 10M), arachidonic acid (0.5mM) and collagen (2g/mL) were used as agonists. PRP was activated with 0.8 unit/ mL thrombin for subsequent ELISA assays of TXB2 (Thromboxane B2), TGF-β (Transforming Growth Factor-Beta) and CD40L (CD 40 Ligand). RESULTS: By Diabetic Status: a.) Baseline platelet aggregations, ATP release and ELISAs were similar between diabetic and non-diabetic subjects, with the exception of platelet aggregation using 5 uM and 10uM as agonist. b.) Mean maximum platelet aggregation after aspirin alone was 20% higher among diabetic subjects. lp;&0.5qAmong all Subjects: a.) Mean TXB2 release among all subjects was reduced from a baseline of 42,075 ± 4,479 pg/ml to 32,719 ± 3,589pg/ml after pioglitazone alone (p = 0.0004). b.) Mean TXB2 release after aspirin alone was 20,829 ± 2,753 pg/ml which was reduced to 9,569 ± 1,653 pg/ml after the addition of pioglitazone (p = 0.0001). (Figure 1) c.) Twenty-five of 40 subjects (63%) had aggregation of greater than 20% using arachidonic acid as agonist despite ingestion of 81 mg aspirin. This decreased to 11 /40 (28%) after the administration of 30 mg of pioglitazone (p < 0.0001). (Figure 2) No significant effects were observed on release of CD40L or TGFβ. Conclusion: Pioglitazone has a direct platelet stabilizing effect and potentiates the effect of aspirin irrespective of underlying cardiovascular risk. Disclosures: Francis: Takeda Pharmaceuticals North America, Inc.: Research Funding.

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.

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

Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

2004 ◽  
Vol 92 (07) ◽  
pp. 89-96 ◽  
Author(s):  
David Payne ◽  
Chris Jones ◽  
Paul Hayes ◽  
Sally Webster ◽  
A. Naylor ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Platelet Inhibition ◽  
Aspirin Resistance ◽  
Arachidonic Acid Metabolism ◽  
Significant Rise ◽  
Control Group

SummaryThe majority of patients who suffer peri-operative thromboembolic complication while undergoing vascular procedures do so despite taking aspirin. This study examined the antiplatelet effect of aspirin during surgery in patients undergoing carotid endarterectomy (CEA). Fifty patients undergoing CEA were standardised to 150 mg aspirin daily for ≥2 weeks. Platelet aggregation in response to arachidonic acid (AA) was measured in platelet rich plasma prepared from blood taken prior to, during, and at the end of surgery. Spontaneous platelet aggregation was also studied, as was the role of physiological agonists (ADP, collagen, thrombin, and epinephrine) in mediating the in vivo and in vitro responses to AA. Eighteen patients undergoing leg angioplasty, also on 150 mg aspirin, without general anaesthesia, served as a control group. In the CEA patients aggregation induced by AA (5 mM) increased significantly from 7.6 ± 5.5% pre-surgery to 50.8 ± 29.5% at the end of surgery (p <0.0001). Aggregation to AA was even greater in samples taken mid-surgery from a sub-set of patients (73.8 ± 7.2%; p = 0.0001), but fell to 45.9 ± 7.4% by the end of surgery. The increased aggregation in response to AA was not due to intra-operative release of physiological platelet agonists since addition of agents that block/neutralise the effects of ADP (apyrase; 4 µg/ml), thrombin (hirudin; 10 units/ml), or epinephrine (yohimbine; 10 µM/l) to the samples taken at the end of surgery did not block the increased aggregation.The patients undergoing angioplasty also showed a significant rise in the response to AA (5 mM), from 5.6 ± 5.5% pre-angioplasty to 32.4 ± 24.9% at the end of the procedure (p <0.0001), which fell significantly to 11.0 ± 8.1% 4 hours later. The antiplatelet activity of aspirin, mediated by blockade of platelet arachidonic acid metabolism, diminished significantly during surgery, but was partially restored by the end of the procedure without additional aspirin treatment.This rapidly inducible and transient effect may explain why some patients undergoing cardiovascular surgery remain at risk of peri-operative stroke and myocardial infarction.

Enhanced Platelet Aggregation And Arachidonic Acid Metabolism Associated To Reduced Sensitivity To Exogenous Prostacyclin In Hypercholesterolemic Subjects

1981 ◽  
Author(s):  
E Tremoli ◽  
P Maderna ◽  
S Colli ◽  
M Sirtori ◽  
C R Sirtori
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Arachidonic Acid Metabolism ◽  
Type Ii ◽  
Thrombotic Risk ◽  
Cholesterol Levels ◽  
Clinical Series ◽  
Age And Sex

The platelet sensitivity to aggregating agents and the production of arachidonic acid (AA) metabolites were studied in 97 hypercholesterolemic patients (WHO types IIA and IIB;serum cholesterol levels >250 mg/dl, LDL>170 mg/dl,triglycerides >180 mg/dl). The findings were compared with those of 55 age and sex matched normocholesterolemic subjects.Platelet aggregation was studied in platelet rich plasma (PRP) with ADP, collagen, epinephrine and thrombofax* as aggregating agents. Malondialdehyde (MDA) production was determined according to Smith et al.. Thromboxane B2 (TXB2) was measured in washed platelets stimulated with AA by a specific RIA. The platelet sensitivity to the inhibitory effect of synthetic prostacyclin (PGI2) was also assessed in 40 of the patients and in 20 age and sex matched control subjects, using fixed concentrations of aggregating agents.Platelets from patients required to aggregate significantly lower concentrations of collagen, epinephrine and thrombofax* (p< 0.001) and of ADP ( p<O.05); MDA production by thrombin and collagen and TXB formation were significantly raised (p<0.001) in the patient group. Higher concentrations of PGI2 were required to inhibit the aggregation of platelets in the type II patients.The reported findings confirm in a large clinical series the potential role of platelet hyperreactivity in the thrombotic risk of type II hypercholesterolemia.

Comparison of Rapid Platelet Function Assay with Whole Blood Platelet Impedance Aggregometry for the Definition of Aspirin Resistance.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4018-4018
Author(s):  
Anna M. Dyszkiewicz-Korpanty ◽  
Anne Kim ◽  
James D. Burner ◽  
Eugene P. Frenkel ◽  
Ravindra Sarode
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Blood Platelet ◽  
Aspirin Resistance ◽  
Impedance Aggregometry ◽  
Definition Of ◽  
Induced Aggregation

Abstract The reported incidence of aspirin (ASA) resistance ranges from 5 to 30%. Various platelet function assays have been employed to detect aspirin resistance in patients with cardio- and cerebrovascular disease. Such a high proposed incidence of ASA resistance poses a critical need for a rapid point-of -care (POC) platelet function test. Unfortunately, no uniformly accepted definition of ASA resistance exists. Platelet aggregation studies that have been used to define ASA resistance are time consuming and require special technical expertise. The Ultegra Rapid Platelet Function -ASA (RPFA-ASA) has been developed as a POC test that is performed without sample processing. This optical method measures agglutination of fibrinogen-coated beads upon platelet activation with arachidonic acid. In the presence of aspirin effect, however, the agglutination of the beads is inhibited. The described cutoff of ≥ 550 Aspirin Reaction Units (ARU) is termed non-responsiveness to ASA based on a preclinical study and subsequent correlation with epinephrine-induced platelet aggregation in platelet rich plasma. Since RPFA-ASA uses whole blood, we validated its performance characteristics against a classic whole blood platelet aggregation assay (WBA). We studied 50 healthy volunteers, aged 25–75 (24 men, 26 women) with normal CBC, who had not ingested anti-platelet drugs for 14 days prior to the study. Baseline studies included WBA (dual channel aggregometer, Chrono-log Inc., Havertown, PA) using both arachidonic acid (AA -0.5; 0.25 mM) and collagen (1; 2 μg/mL) as well as an RPFA-ASA assay (Accumetrics Inc., San Diego, CA). These studies were repeated after 3 days of ASA (325 mg/d) intake. Based on a review of the literature, we defined an adequate ASA response as a completely inhibited AA-induced platelet aggregation and at least 30% inhibition of collagen-induced aggregation (both concentrations of the agonist). Thus, those with &lt; 30% inhibition of aggregation response to collagen were considered ASA resistant. Eleven subjects were ASA resistant by WBA (20%; 8 females and 3 males (aged 25–63). In contrast, since all 50 subjects achieved ARU values of &lt; 550 ARU, none were recognized as an ASA non-responder by the RPFA-ASA. While the current cutoff of &lt; 550 ARU posed by the Ultegra RPFA-ASA does identify those who have taken ASA, the assay is unable to recognize ASA non-responders. Thus, based on these data, the appropriate cutoff for the recognition of ASA resistance by the RPFA-ASA should be re-adjusted to a significantly lower level to ensure appropriate assay results.

CYCLOOXYGENASE AND LIPOXYGENASE PRODUCTS SYNERGISTICALLY MODULATE TUMOR CELL INDUCED PLATELET AGGREGATION

1987 ◽  
Author(s):  
Bruce W Steinert ◽  
James M Onoda ◽  
Bonnie F Sloane ◽  
John D Taylor ◽  
Kenneth V Honn
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Tumor Cell ◽  
Acid Metabolism ◽  
Platelet Rich Plasma ◽  
Arachidonic Acid Metabolism ◽  
Cyclooxygenase Inhibitors ◽  
Dependent Manner ◽  
Lipoxygenase Inhibitors ◽  
Agonist Concentration

There has been considerable controversy surrounding the ability of inhibitors of arachidonic acid metabolism to concomitantly inhibit tumor cell induced platelet aggregation (TCIPA). Reconciliation of this controversy has been difficult due to the wide variability of experimental conditions (e.g., inhibitor concentration, strength of the inducing agonist).In the present study, we examined the effects of several cyclooxygenaseand lipoxygenase inhibitors on the induction of platelet aggregation by Walker 256 carcinosarcoma (W256) cells. We have previously demonstrated that aggregation of platelet rich plasma (PRP), induced by W256 cells, was initiated via a thrombin dependent mechanism. Platelet aggregation was induced by the addition of W256 cells (75,000-J500,000 cells/cuvette) to rat PRP preincubated with inhibitor(s) or diluent. The strength of the inducing stimulus affected both the degree of aggregation and the production of thromboxane A2 (TXA2) in a dose dependent manner. A weak stimulus (low concentration of W256 cells) produced only a low level of aggregation and low TXA2 production, whereas aggregation induced by a strong stimulus (high concentration of W256 cells) resulted in significant aggregation and increased TXA2 production. Preincubation (5 min., 37°C) of rat PRP with cyclooxygenase inhibitors (e.g., aspirin, indomethacin, ibuprofen) resulted in complete inhibition of platelet aggregation at low agonist concentration (75,000 W256 cells), whereas when a high agonist concentration (500,000 W256 cells) was used to induce aggregation, the inhibitors failed to inhibit TCIPA. The addition of fewer than 50,000W256 cells failed to induce any measurable platelet aggregation in the presence or absence of inhibitors. TCIPA was not affected by lipoxygenaseinhibitors (e.g.,quercetin) alone regardless of agonist concentration. Both cyclooxygenase and lipoxygenase inhibitors, however, were required to significantly inhibit TCIPA induced by high agonist concentration. Compounds which inhibited both the cycloogygenase and lipoxygenase pathways (e.g.,hydroquinone, BW755c) inhibited TCIPA at all agonist concentrations. Nafazatrom failed to inhibit TCIPA consistant with a lack of effect on platelet cyclooxygenase and lipoxygenase. Therefore, we conclude cyclooxygenase (e.g., TXA2) and lipoxygenase (e.g., 12-HETE) products of platelet arachidonic acid metabolism and the strength of the inducingagonist are important criteria in TCIPA. This study may help to clarify the current controversy regarding the inhibition of TCIPA by inhibitors of arachidonic acid metabolism.

scholarly journals Arachidonic Acid Metabolism of Platelet in Diabetes

1977 ◽  
Author(s):  
T. Kurosawa ◽  
T. Tojima ◽  
H. Funayama ◽  
Y. Takahashi ◽  
Y. Shiokawa
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Sodium Citrate ◽  
Acid Metabolism ◽  
Platelet Rich Plasma ◽  
Normal Subjects ◽  
Arachidonic Acid Metabolism ◽  
Gas Liquid Chromatography ◽  
Glucose Loading ◽  
Freeze Dried

Recent reports have indicated that platelet aggregation is enhanced in some diabetics who have proliferative retinopathy and that platelet function is a altered by glucose loading. But the mechanism is not clarified yet. Arachidonic acid, the precursor of prostaglandin endoperoxide, plays a major role on platelet aggregation. Blood samples were collected with sodium citrate at 0, 30, 60, 120 and 300 minutes after 100 g glucose loading. Platelet-rich plasma was obtained by centrifugation and platelet aggregation was studied photometrically adding ADP. Platelet was obtained by further centrifugation and was kept freeze-dried. Platelet samples were extracted and transesterificated and separated by gas liquid chromatography. The quantitative regulation of arachidonic acid in platelets was measured by the composition ratio of arachidonic acid (C20-4)/linoleic acid (C18-2)=AL index. The results of platelet aggregation after glucose loading were as follows; platelet aggregation was not changed remarkably in normal subjects, but was enhanced at 30 and 60 and suppressed at 120 minutes in diabetics.AL index is as fol lows:prior to glucose loading, AL index of diabetics (4.6 ± 1.2) was higher than that of normal subjects (3.5 ± 0.5). After glucose loading, no significant change was observed in normal subjects, but AL index was increased at 30 (4.8 ± 1.4) and 60 (4.9 ± 1.4) and decreased at 120 minutes (4.1 ± 0.9) in diabetics. The results indicates that there is a certain relationship between quantitative regulation of arachidonic acid in platelet and platelet aggregation and that hyperaggregation may be induced by abnormal prostaglandin metabolism in diabetes.

Investigation of Platelet Functions in Chronic Myeloproliferative Disorders by Optical and Luminesance Method.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4766-4766
Author(s):  
Meltem O. Akay ◽  
Fezan S. Mutlu ◽  
Zafer Gulbas
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Reference Range ◽  
Platelet Rich Plasma ◽  
Atp Release ◽  
Adenosine Diphosphate ◽  
Myeloproliferative Disorders ◽  
Test Results ◽  
Chronic Myeloproliferative Disorders ◽  
Significant Difference

Abstract Background: Bleeding and thrombosis are common causes of morbidity and mortality in patients with myeloproliferative disorders (MPD). Qualitative platelet abnormalities are frequently found in these patients and range from platelet hypofunction as demonstrated by defective invitro platelet aggregation, acquired storage pool disease and/or platelet membrane defects, in addition to enhanced platelet aggregation, increased plasma beta thromboglobulin levels or shortened platelet survival. In this study we aimed to perform platelet aggregation studies by optical method (on platelet rich plasma=PRP) and luminesance method (on whole blood) in chronic myeloproliferative disorders. Methods:A total of twenty-five patients with MPD (17 chronic myeloid leukemia, 6 polycythemia vera, 2 essential thrombocytosis) were enrolled. Median age was 54,4 (29–76). Platelet aggregation was measured using the optic and luminesance method. The agonists used were adenosine diphosphate (ADP), arachidonic acid (AA) ristocetin and collagen. Platelets were considered to be hyperactive if at least one result (i.e. aggregation or ATP release with one agonist) was above the reference range, and hypoactive if at least one result (i.e. aggregation or ATP release) was below the reference range. Mixed hypo- and hyperactive platelets were considered present when at least one result (i.e. aggregation or ATP release) was below and above the reference range respectively. Results:Platelet aggregation test results by two methods in myeloproliferative disorders were shown in Table 1. The percent for detection of platelet function abnormality by luminesance method was found to be higher than the optic method and a significant difference was shown between two methods (p&lt;0,05). Conclusion Our findings suggest that;1. Luminesance platelet aggregation study is more valuable than optic platelet aggregation study for invitro assessment of platelet function in patients with MPD. 2. The use of luminesance platelet aggregation study appears useful to select patients for antiplatelet therapy. Platelet aggregation test results in myeloproliferative disorders (n=25) Normal Hypofunction Hyperfunction Mix Total abnormality Luminesance method 1(%4) 4(%16) 8(%32) 11(%44) 24(%96) Optic method 9(%36) 11(%44) 2(%8) 3(%12) 16(%64)

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.

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