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PubMed2002

Determinants of platelet aggregation in 50-70-year-old men from three Japanese communities.

To investigate the association of lifestyle and constitutional variables with platelet aggregation, we examined the platelet aggregation, serum fatty acid composition, alcohol intake, smoking, and dietary intake of seafood and soybean estimated by a 1-week dietary record in 448 males aged 50-70 in three rural Japanese communities: Ikawa, Akita prefecture (northeast coast), Noichi, Kochi prefecture (southwest coast), and Kyowa, Ibaraki prefecture (central inland). Platelet aggregatory threshold index (PATI) was used to determine the minimum concentration of adenosine 5'-diphosphate (ADP) that caused a non-reversible aggregation of platelets. Intake of seafood and n3-polyunsaturated fatty acid and ingestion of ethanol were higher in the northeast coastal community than in the other two communities. Mean platelet and white blood cell counts were lower in northeast coastal community than in the other two communities. The geometric mean PATI was higher (i.e. platelet aggregation was lower) in the northeast coastal community than the other two communities. Within the entire sample, platelet aggregation correlated inversely with serum level of n3-polyunsaturated fatty acids and gamma-glutamyl transpeptidase, an index of alcohol consumption, and positively with platelet and white blood cell counts. Platelet aggregation tended to correlate positively with serum arachidonic acid. There was no correlation between smoking and platelet aggregation. Our results suggest that seafood intake and moderate alcohol consumption reduce platelet aggregation.

Aged↗
PubMed1981

A method for quantitating platelet aggregation and analyzing drug-receptor interactions on platelets in whole blood in vitro.

A method for quantitating platelet aggregation in whole blood is described. The method is rapid and reproducible. By utilizing the Ultra-Flo 100 whole blood platelet count, platelet numbers before and after addition of an aggregating agent are counted electronically, without the need to separate platelets from other blood cell types. Although designed primarily for use with human blood, the Ultra-Flo can also be used successfully with blood from other species. The method has been used to study the antagonism of adrenaline-induced aggregation of platelets in human whole blood by the alpha-adrenoceptor blocking drug phentolamine. The potential of the method for studying drug-receptor interactions on platelets in vitro as well as rapid assessment of platelet function ex vivo is discussed.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2004

Achieved platelet aggregation inhibition after different antiplatelet regimens during percutaneous coronary intervention for ST-segment elevation myocardial infarction.

OBJECTIVES: To evaluate the extent of platelet aggregation inhibition in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI), treated with different antiplatelet agents and dosages. BACKGROUND: The extent of platelet aggregation inhibition is an independent predictor of major cardiac events after elective PCI. In STEMI patients undergoing PCI, routine dose of antiplatelet agents may be associated with less effective platelet aggregation inhibition. METHODS: Patients were treated with clopidogrel before angiography and randomized to abciximab, tirofiban, high-dose tirofiban, or no glycoprotein (GP) IIb/IIIa inhibitor; GP IIb/IIIa inhibitor bolus, followed by maintenance infusion, was administered after angiography, but before PCI. Platelet aggregation inhibition was assessed before angiography, immediately after PCI, and 1 and 6 h afterwards. RESULTS: The total study population consisted of 112 patients. Platelet aggregation inhibition was variable for individuals and suboptimal for all agents, particularly in the periprocedural period. Only with high-dose tirofiban, mean periprocedural platelet aggregation inhibition exceeded 80%. Angiographic parameters after PCI were not different between the groups. No relationship was found between the level of platelet aggregation and parameters of PCI success (Thrombolysis In Myocardial Infarction frame count and myocardial blush grade), after combining the data from all four groups studied. CONCLUSIONS: Platelet aggregation inhibition in STEMI patients undergoing PCI, treated with antiplatelet agents, is variable and suboptimal for all agents and dosages studied. Only with high-dose tirofiban, mean periprocedural platelet aggregation inhibition exceeded 80%. However, no relationship of platelet aggregation inhibition and angiographic outcome was found in this patient cohort.

Abciximab↗
PubMed1988

Some novel inhibitors of platelet aggregation: acute toxicity in mice and its relationship to in vitro activity and toxicity.

Five carbamoylpiperidine congeners and one nipecotoylpiperazine derivative, which inhibit ADP-induced aggregation of human blood platelets in vitro, were evaluated in vivo for acute toxicity to male and female ICR mice. Although the in vitro platelet aggregation inhibiting potency of these compounds covered about a 1150-fold range, the acute ip LD50s (microM/kg) in mice showed only a fourfold range of values. An increase in platelet aggregation inhibiting potency (in vitro) was not paralleled by an increase in acute toxicity in vivo for these compounds; in fact, the most potent aggregation inhibitor (microM/liter) was the least toxic (microM/kg) to mice. A comparison of acute LD50s (microM/kg) to concentrations which produce 50% inhibition of mouse fibroblast cell growth in culture (microM/liter) did not yield a consistent value, nor was the rank order of toxicity the same from these two tests. In hematoxylin and eosin stained slides of major organs from treated mice, no histopathologic lesions were observed which were attributable to administration of these compounds.

Animals↗
PubMed2005

Effects of different aspirin formulations on platelet aggregation times and on plasma salicylate concentrations.

BACKGROUND: Early aspirin treatment is widely used to inhibit platelet activity and to reduce morbidity and mortality in patients presenting with an acute myocardial infarction or a stroke. A number of different aspirin formulations have been used for this purpose; however, a comparison of their effectiveness in inhibiting early platelet aggregation has not been determined. METHODS: In this study, we determined plasma salicylate concentrations and platelet inhibitory activities at various times after ingestion of three commonly used aspirin formulations: soluble aspirin (Alka-Seltzer), 325 mg, chewed baby aspirin, 324 mg, and whole compressed non-enteric coated aspirin, 324 mg. Twenty-four healthy volunteers, 18-39 years of age, participated in the prospective single-blinded triple-crossover study. Plasma salicylate concentrations and inhibition of arachidonic acid-induced platelet aggregation were determined on post-dose blood samples collected at 2.5, 5.0, 7.5, 10, 15, 20, 25, 30, and 40 min. All subjects crossed over to the other two formulations with at least 2 weeks between ingestions. RESULTS: The median platelet inhibition times for the chewed, soluble, and whole aspirin formulations were 7.5, 7.5, and 10.0 min, respectively. Soluble and chewed aspirin were found to inhibit platelet aggregation faster than whole aspirin (p<0.001); however, there were no significant differences in platelet aggregation times between the soluble and chewed formulations (p<0.163). Inhibition of platelet aggregation was found to occur at an average plasma salicylate concentration of 2.46 microg/mL, regardless of method of ingestion. CONCLUSION: The results indicate that soluble and chewed aspirin inhibit platelet aggregation in a shorter period of time than does whole aspirin. The results suggest that chewing baby aspirin or taking soluble buffered aspirin may be the preferred route of administration for early platelet inhibition.

Administration, Oral↗
PubMed1992

Spontaneous platelet aggregation in thalassemic children and adolescents.

Spontaneous platelet aggregation was studied in 51 children and adolescents, comprising 30 nonsplenectomized thalassemic patients, 12 splenectomized thalassemic patients and 9 normal children. Spontaneous platelet aggregation was significantly increased in whole blood and platelet-rich plasma of splenectomized thalassemic patients but not in nonsplenectomized cases.

Adolescent↗
PubMed1996

Blood coagulation and platelet aggregation in major depression.

Recently, it was found that the plasma of depressed patients significantly reduced the primary and secondary platelet aggregation to aggregating agents, such as ADP and collagen, in platelet rich plasma (PRP) of normal volunteers. Other authors found significantly decreased maximum amplitudes of adrenaline-induced platelet aggregation in major depressed patients versus normal controls. The aim of the present study was to examine platelet aggregation and blood coagulation in depression. Toward this end, the authors have measured secondary platelet aggregation to ADP and collagen, and the activated partial thromboplastin time (APTT) and prothrombin time (PT) in 16 normal volunteers, 16 minor, 40 simple major and 23 melancholic subjects. There were no significant differences in ADP- or collagen-induced platelet aggregability, APTT or PT between normal controls, minor, simple major or melancholic depressed patients. There were no significant relationships between severity of depression and APTT, PT or platelet aggregability to ADP or collagen. It is concluded that blood coagulation and platelet aggregability to ADP and collagen are probably not disordered in major depression.

Adult↗
PubMed2002

Influence of spontaneous platelet aggregation on progression of glomerular disease.

UNLABELLED: Platelet secretion products may play an important role in the pathogenesis and progression of the kidney disease. Amongst the parameters describing platelet hyperactivity the measurement of spontaneous platelet aggregation (SPA) seems particularly useful. In this study SPA as well as mean platelet volume (MPV), modal platelet volume (PLT Mode) and platelet count (PLT) were investigated in 60 patients with biopsy proven primary glomerulonephritis. SPA was measured using the turbidimetric method according to Born with no enhancers added. Serum creatinine concentration (Cr), reciprocal serum creatinine concentration (1/Cr) and endogenous creatinine clearance (Cl(Cr)) were used for the renal function estimation. Protein and lipid profiles as well as coagulo-fibrinolytic balance were measured in parallel. The investigated group consisted of 30 non-nephrotic patients (CGN) - in 9, SPA was found (CGN-B) while 21 had SPA <10% (CGN-A), and 30 nephrotic patients (CGN+NS) - 19 with SPA (CGN+NS-B) and 11 without (CGN+NS-A). SPA was found to be a constant platelet feature in patients with chronic glomerulopathy. The group remained under observation for 36 months. 41 patients were included in the 3-year prospective study which revealed the significant influence of the blood platelet hyperaggregability on the renal disease progression. A significantly increased serum creatinine concentration, decreased 1/Cr parameter and decreased glomerular filtration rate (Cl(Cr)) were noted in subgroups showing SPA. A significant correlation between SPA and (Delta)Cr/month (r = 0.41), (Delta)1/Cr/month (r = 0.38) as well as (Delta)Cl(Cr)/month (r = 0.52) was found. The platelet activity and thus SPA can be altered by various factors: albumin and fibrinogen plasma concentrations, thrombosis activation and possibly lipoprotein metabolism disturbances. A characteristic feature of spontaneously aggregating platelet is their increased volume (MPV). CONCLUSION: Platelet hyperaggregation in one of nonimmunological factors stimulates the progression of glomerulonephritis.

Adult↗
PubMed1996

Effect of quercetin on platelet aggregation induced by oxyradicals.

AIM: To study the action of quercetin (Que) on inhibiting platelet aggregation. METHODS: Active oxygen free radicals produced by xanthine/xanthine oxidase (Xan/XO) reaction was used, platelet aggregation was determined by the turbidimetric method, and the Xan/XO oxyradicals generating reaction by luminol-dependent chemiluminescence (Che) method. RESULTS: Active oxygen free radicals enhanced the platelet aggregation induced by ADP 1.6 mumol.L-1. The rate of maximal aggregation increased from 29%-38% for ADP to 59%-70% for ADP + Xan/XO. The enhancement was abolished by the treatment of platelet-rich plasma (PRP) with Que 650 mumol.L-1 or hydrocortisone (Hyd) 900 mg.L-1. Both Que and Hyd scavenged the active oxyradicals in vitro. The Che was decreased by 75.7% (Que 4 mumol.L-1) and 79.0% (Hyd 900 mg.L-1) as compared with control. CONCLUSION: Active oxygen free radicals participated in the platelet aggregation, and scavenging oxyradicals by Que was one of mechanisms of inhibiting platelet aggregation.

Animals↗
PubMed1992

Increased whole blood platelet aggregation in normal pregnancy can be prevented in vitro by aspirin and dazmegrel (UK38485).

OBJECTIVE: To determine the effect of normal pregnancy and the early puerperium on whole blood platelet aggregation and to assess the role of thromboxane A2 (TXA2) in platelet aggregation in pregnancy. DESIGN: A prospective descriptive study. SETTING: TCD Medical School, St James's Hospital, Dublin. SUBJECTS: Twenty healthy primigravidae who remained normotensive during pregnancy and the puerperium. INTERVENTIONS: 20 ml blood samples were obtained serially at 12, 20, 28, 32 and 36 weeks gestation, during established labour and at 1 h, 24 h, 48 h and 6 weeks after delivery. MAIN OUTCOME MEASURES: Whole blood platelet aggregation in response to aggregating agents ADP, PAF (platelet aggregating factor) collagen, adrenaline and arachidonic acid (AA) at each stage of pregnancy and peuerperium was measured using a particle counting technique. The in vitro effect of aspirin and dazmegrel (thromboxane synthetase inhibitor UK38485) on platelet aggregation in pregnancy was also investigated. RESULTS: Platelet aggregation in response to collagen, adrenaline, ADP and AA were increased in the last trimester, during labour and at 1 h after delivery but decreased 24-48 h after delivery. Platelet aggregation in response to AA, collagen and adrenalin was reduced by both aspirin and dazmegrel. CONCLUSIONS: The earliest and most marked increases in platelet aggregation during normal pregnancy were found in response to AA and collagen. These platelet changes were prevented when whole blood was pre-incubated with either aspirin or dazmegrel. This suggests that enhanced production of TXA2 is responsible for increased platelet reactivity in normal pregnancy.

Adenosine Diphosphate↗
PubMed2003

Differential effect of aspirin on platelet aggregation in patients with coronary artery disease in relation with associated risk factors.

Platelets play a key role in the pathogenesis of atherosclerosis and acute coronary syndromes and antiplatelet therapy offers a clinical benefit. Although aspirin is the most widely used agent, there are several conditions in which aspirin may fail to provide a full antithrombotic benefit. Furthermore, data concerning the relationship between platelet function, aspirin, and the associated risk factors are limited. In the present study. ADP and collagen-induced platelet aggregation of 200 consecutive patients with suspected coronary artery disease (CAD) who underwent coronary angiography were evaluated. The patients were classified into three groups according to the number of stenotic vessels. One hundred and eight patients were using 300 mg/day of aspirin. The associated cardiovascular risk factors were also considered. The collagen-induced platelet aggregation of smokers was significantly higher than non-smokers (P < 0.05). Although platelet aggregation was higher in diabetic and hypertensive patients, the difference was not statistically significant. No significant correlation was found between platelet aggregation and other risk factors. The collagen-induced platelet aggregation of the subjects with non-stenotic vessels was reduced by aspirin (P < 0.05). Aspirin did not sufficiently inhibit ADP and collagen-induced aggregation in patients with CAD. This finding supports the idea that the nonplatelet-mediated effects of aspirin could be more important than its antiplatelet effect in clinical use and the use of new potent antiplatelet drugs may complete its antiplatelet effect.

Adult↗
PubMed1994

Compliance with antiplatelet therapy in patients with ischemic cerebrovascular disease. Assessment by platelet aggregation testing.

BACKGROUND AND PURPOSE: Antiplatelet therapy is currently one of the methods for preventing transient ischemic attacks and cerebral thrombosis. Because antiplatelet agents are generally administered on a long-term basis, patient compliance is an important factor. The purpose of this study was to determine the compliance of patients during antiplatelet therapy by testing platelet aggregation. METHODS: To establish the conditions for measuring platelet aggregation, the platelet aggregation test was performed in patients taking 81 mg/d aspirin or 200 mg/d ticlopidine at the following final concentrations of aggregation-inducing agents: 0.5, 1, 2, and 4 mumol/L ADP and 0.5 and 2 micrograms/mL collagen. The optimum measurement conditions for assessing patient compliance were determined. Under the conditions determined in the first study, platelet aggregation was assessed, and the effects of treatment were studied in 159 outpatients and 79 inpatients undergoing antiplatelet therapy. If the antiplatelet effect was insufficient, compliance was checked by interview. RESULTS: The agents used and the final concentrations found to be optimum for assessing platelet aggregation were 2 micrograms/mL collagen for patients taking aspirin 81 mg/day and 2 mumol/L ADP for patients taking ticlopidine 200 mg/d. In 17 (10%) of the 159 outpatients, platelet aggregation was not adequately reduced because of noncompliance with their antiplatelet therapy. CONCLUSIONS: This study indicated that monitoring of compliance is important for outpatients on antiplatelet therapy. It is best if platelet aggregation can be checked, but when this is impossible it is necessary to assess compliance periodically and provide patient guidance.

Adenosine Diphosphate↗
PubMed1992

Effect of prostaglandin E2 and 3-morpholinosydnonimine (SIN-1) on arachidonic acid metabolism in fMLP-stimulated rat neutrophils and on thrombin-induced human platelet aggregation.

The effects of prostaglandin (PG) E2 and the nitric oxide (NO) donor SIN-1 on leukotriene (LT) release from formyl-methionyl-leucyl-phenylalanine (fMLP) (100 nM)-stimulated rat peritoneal neutrophils (RPN) and on thrombin-induced aggregation of washed human platelets were investigated. Both PGE2 (1-100 nM) and SIN-1 (30-300 microM) inhibited release of LTB4 and cysteinyl-LT from RPN in a concentration-dependent manner. The combined effects of PGE2 and SIN-1 were not greater than expected by summation. On the other hand, the inhibitory effect of SIN-1 (0.5 or 1.0 microM) on platelet aggregation was potentiated by PGE2 (0.3-5 microM) in a concentration-dependent manner, while PGE2 alone in the concentrations used had only marginal effects. The results suggest differential regulation of platelet and leukocyte functions by the mediators PGE2 and NO, which could be relevant for various physiological and pathophysiological conditions.

Animals↗
PubMed2004

In vivo effect of losartan on platelet aggregation in patients with hypertension.

The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 +/- 12.8 and 149.2 +/- 17.3 mmHg, respectively. Mean DBP decreased from 93.7 +/- 8.2 to 87.7 +/- 10.3 mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% +/- 24.3% before and 58.3% +/- 18.1% after the treatment. The same variables with ristocetin were 66.8% +/- 21.6% and 60.8% +/- 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.

Adenosine Diphosphate↗
PubMedDate not supplied

A study of platelet aggregation and adhesion in gout.

Platelet aggregation and adhesion were measured in twelve male patients with gout. Tests were performed with the patients off all treatment for six weeks and after the serum uric had been lowered with allopurinol. Results of aggregation and adhesion tests were normal and not influenced by the uric acid level. The increased cardiovascular disease risk in gout is unlikely to be due to an increased thrombotic tendency.

Adult↗
PubMed1989

Isolation and effects of some garlic components on platelet aggregation and metabolism of arachidonic acid in human blood platelets.

Effects of aqueous extract of garlic, of materials extracted in two organic solvents, viz., ether and chloroform in succession, and of some fractions obtained after TLC of the aqueous extract were examined on platelet aggregation induced by several aggregating agents. Their effects were also investigated on the formation of thromboxane and lipoxygenase products from endogenous arachidonic acid in intact platelets. The aqueous extract inhibited aggregation induced by all aggregating agents and so did the materials extracted in two organic solvents. Only two fractions obtained from TLC of the aqueous garlic extract were examined for effects on epinephrine- and arachidonic acid (AA)-induced aggregation; they were found to be antiaggregatory. The material extracted in ether (MEE) inhibited the incorporation of labelled AA into platelets in platelet-rich plasma. Garlic extracts (MEE and material extracted in chloroform, MEC) at higher dosage inhibited the degradation of platelet phospholipids and reduced the formation of thromboxane (TxB2) and lipoxygenase-derived products from labelled platelets. The two organic extracts at low dosage, while not affecting the degradation of platelet phospholipids, inhibited the cyclooxygenase and lipoxygenase enzymes. A concomitant increase in the amount of released AA was observed in the treated platelets. Similar effects in relation to dosage were observed with the aqueous extract of garlic.

Arachidonic Acid↗
PubMed1975

Platelet aggregability in relation to impaired consciousness after head injury.

ADP-induced platelet aggregation was studied for up to six weeks in 34 patients with head injuries. The patients were divided into three groups according to the degree of impaired consciousness assessed by a clinical coma scale, and change in platelet aggregation was related to the coma score. Platelet aggregation was markedly reduced in all eight patients dying within 24 hours of injury. All 17 patients who remained unconscious for four days or more showed decreased platelet aggregation up to nine days after admission, the most marked effect being on the second day. Platelet function in this group returned to normal within 16 days. Nine patients with only slightly impaired consciousness also showed subnormal platelet aggregation during the first few days with a return to normal by the fourth day. Platelet counts remained within normal limits in all groups. We suggest that during coma following head injury brainstem dysfunction induces neurohumoral changes in the blood which are responsible for a decrease in platelet function.

Adenosine Diphosphate↗
PubMed1997

Platelet aggregation and lipid profile in offsprings of young ischemics.

OBJECTIVE: To study the platelet aggregation and lipid profile in offsprings of young ischemic parents. DESIGN: Cross sectional. SETTING: Hospital based. METHODS: 40 adults under 45 years of age with proven CHD and their 50 offsprings comprised the study group. In the control group, 40 age matched adults with normal maximal treadmill test and their 50 off springs were included. All were screened for lipid profile and platelet aggregation. RESULTS: Platelet aggregation was significantly elevated in adults with CHD (44.0 +/- 15.5%) compared to controls (32.22 +/- 9.1%). Children of CHD adults also had significantly elevated aggregation (34.9 +/- 12.5%) compared to control offsprings (27.8 +/- 9.9%). Adult CHD subjects had significantly elevated serum cholesterol, LDL-cholesterol (LDL-C) and atherogenic index compared to control adults. The children in both groups had similar lipid profiles. CONCLUSION: Platelet aggregation is enhanced in offsprings of young ischemics. The potential of this index as a marker for early development of CHD needs to be explored.

Adolescent↗