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PubMed1983

[Demonstration of spontaneous platelet aggregation and research on circulating platelet aggregates: methodology, results and significance].

136 control subjects and 131 patients, consisting of 23 diabetics with severe retinopathy, 43 cases of valvular disease with or without a prosthesis and 65 patients who had a cerebral vascular accident, were systematically investigated for the presence of spontaneous platelet aggregation 31 controls and 108 patients were examined for reversible circulating platelet aggregates using the technique of Wu and Hoak. Frank spontaneous aggregation was observed in 6 of the 136 control subjects, 6 of the 21 patients without a valvular prosthesis and 2 of the 22 patients with such a valvular prosthesis and 2 of the 22 patients with such a prosthesis, only 1 of the 23 diabetics and 5 of the 65 patients with old or recent cerebral vascular accidents. The incidence of spontaneous aggregation seems to be directly related to certain operative conditions: the type of machine used, the number of platelets, and to the treatment administered, the Wu and Hoak test. No statistically significant correlation was demonstrated between spontaneous aggregation and the Wu and Hoak test. The exact clinical significance of the presence of spontaneous aggregation is still disputed. However, the examination for this abnormality should be routine as its presence can alter the interpretation of the results of aggregation induced by various aggregating agents.

Blood Platelets↗
PubMed1995

[Shear-induced platelet aggregation (SIPA) monitoring of hemostatic effect during platelet transfusion in a patient with Glanzmann's thrombasthenia: a comparison between SIPA and conventional platelet aggregation].

Shear-induced platelet aggregation (SIPA) in a patient with Glanzmann's thrombasthenia was examined during platelet infusion therapy. Prior to platelet infusion, SIPA measured with the modified cone-and-plate type viscometer, as well as ADP-and collagen-induced platelet aggregation measured with the conventional platelet aggregometer, were absent. The patient's SIPA after multiple infusions of platelet, in parallel with the bleeding time and the clinical hemostatic effect, improved to the normal level, while ADP-and collagen-induced platelet aggregation remained abnormal. These observations imply that SIPA is physiologically more relevant than the conventional agonist-induced platelet aggregometry in this type of the disease.

Adenosine Diphosphate↗
PubMed2005

Hypertensive patients with carotid artery plaque exhibit increased platelet aggregability.

BACKGROUND: Platelets play an important role in myocardial infarction and ischemic stroke events, but whether platelet aggregability is related to early stage arteriosclerosis remains unclear. METHODS: We used a novel platelet counting system which makes it possible to detect spontaneous platelet aggregation, to evaluate the relationship between platelet aggregability and carotid artery arteriosclerosis in 125 outpatients with primary hypertension (46-73 years old: 65 men, 60 women). All subjects underwent carotid artery ultrasonography to determine whether plaque was present and to estimate intima-media thickness. RESULTS: Patients with carotid artery plaques (Plaque(+), n=63) were older and had higher systolic blood pressures than patients without plaques (Plaque(-), n=62), but no significant differences in sex, body mass index, diastolic blood pressure, plasma concentrations of glucose, total cholesterol, triglyceride, lipoprotein cholesterol, fibrinogen or the platelet count in whole blood were observed between Plaque(+) and Plaque(-) groups. Plaque(+) subjects showed greater spontaneous platelet aggregability and platelet aggregation induced by 2 microM or 0.5 microM of ADP or 0.3 microM of epinephrine than the Plaque(-) group. When age and systolic blood pressure were matched (n=52 in both groups), the Plaque(+) subjects exhibited greater platelet aggregability than the Plaque(-) subjects. Platelet aggregation induced by 2 microM of ADP showed statistical significant positive correlation coefficients with age, HbA1c and diastolic blood pressure. CONCLUSION: Our results indicate that hypertensive patients with carotid artery plaque have increased platelet aggregability. A prospective study is recommended to clarify whether this increase in platelet aggregability promotes the progression of arteriosclerosis.

Adenosine Diphosphate↗
PubMed1995

Calcium-induced platelet aggregation in washed platelets from guinea pigs.

The present study investigated the effects of extracellular calcium on washed platelets of guinea pigs, rabbits, rats and humans. CaCl2 without agonists induced platelet aggregation in guinea pigs and rabbits, but not in rats or humans. CaCl2 increased platelet [Ca2+]i in Fura-2-loaded guinea pig platelets. Calcium-induced platelet aggregation was inhibited by W-7 (a calmodulin antagonist), aspirin, indomethacin, TMB-8 (an inhibitor of intracellular Ca2+ release) and also nicardipine (a calcium antagonist). These data suggest that CaCl2-induced platelet aggregation is mediated by calmodulin, cyclooxygenase and other, as yet unknown, mechanisms.

Animals↗
PubMed1997

Nitric oxide inhalation inhibits platelet aggregation and platelet-mediated pulmonary thrombosis in rats.

Endothelium-derived nitric oxide (NO) inhibits in vitro platelet aggregation via a cGMP-dependent mechanism. The effect of inhaled NO on platelet-mediated pulmonary thrombosis following intravenous thrombotic challenge with collagen was examined in rats and compared with the effect of G4120, a cyclic Arg-Gly-Asp-containing synthetic pentapeptide that binds to the platelet glycoprotein IIb/IIIa receptor. Intraplatelet cGMP dose-dependently increased from 39 +/- 6 fmol/10(8) platelets in control to 46 +/- 6, 68 +/- 13, and 81 +/- 13 fmol/10(8) platelets after inhalation with 20, 40, and 80 ppm NO, respectively (P < .05 for 40 and 80 ppm). Ex vivo platelet aggregation of platelet-rich plasma induced by 1 microgram/mL collagen was reduced from 75 +/- 4% in control rats to 22 +/- 10% and 20 +/- 7% in rats ventilated with 40 and 80 ppm NO, respectively, and to 30 +/- 9% in G4120-treated rats (each P < .05 versus control). Circulating platelet counts 3 minutes after collagen injection were significantly higher in the inhaled NO and G4120 groups compared with control rats (250,000 +/- 18,000 and 223,000 +/- 10,000/microL versus 160,000 +/- 18,000/microL, each P < .05). The rise in pulmonary arterial pressure after collagen injection was significantly reduced in NO- and G4120-treated rats (26 +/- 1 and 27 +/- 1 versus 32 +/- 1 mm Hg in control rats, each P < .05). The number of pulmonary resistance vessels containing platelet thrombi was significantly smaller after inhaled NO and G4120 treatment compared with control (56 +/- 3% and 50 +/- 3% versus 68 +/- 3%, respectively; P < .05). Thus, NO inhalation reduces in vivo activation of circulating platelets and platelet-rich thrombosis in thromboembolic pulmonary hypertension. Inhalation of NO may be useful in cardiovascular diseases associated with platelet activation.

Administration, Inhalation↗
PubMed1991

[Procoagulant and aggregating platelet activities of human mammary tumor cells].

The ability of tumor cells to initiate coagulation, platelet aggregation and subsequent thrombotic alterations is believed to facilitate metastatic process. The mechanisms by which tumor cells develop thrombotic events in malignancy are discussed. We have examined the procoagulant activity and the modifications of rheologic platelet functions induced by 3 human mammary tumor cell lines (MCF-7, ZR-75-1, BT-20) using a laser-thromborheometer. According to experimental conditions, these 3 tumor cell lines aggregate platelets via a thrombin-dependent mechanism. Moreover, MCF-7 cells also induce ADP-like platelet aggregation. These data suggest the existence of several mechanisms of mammary tumor cell-induced platelet aggregation.

Blood Coagulation↗
PubMed1989

Intralipid infusion into humans reduces in vitro platelet aggregation and alters platelet lipid composition.

Intralipid (Kabi Vitrum Inc, Alameda, CA) infusion into normal volunteers results in substantial elevation in serum triglyceride, phospholipids, and free cholesterol concentrations. Platelet aggregation induced in vitro in platelet-rich plasma by collagen or ADP was significantly reduced by up to 40% and 45%, respectively, during the infusion period but returned to preinfusion levels 18 hours after the end of the infusion. In parallel, platelet lipid composition was also affected. Platelet free cholesterol content was reduced by up to 20% during the infusion of Intralipid, whereas platelet triglyceride and phospholipid contents increased by 3.5-fold and twofold, respectively. Eighteen hours after the end of the infusion, both platelet cholesterol and triglyceride returned to preinfusion levels, but platelet phospholipid was still elevated. Both components of Intralipid (liposomes and triglyceride-phospholipid particles) were able to decrease in vitro platelet aggregation and platelet cholesterol content. Our results demonstrate decreased platelet function induced by Intralipid infusion into humans, which was associated with reduced platelet cholesterol content. These results suggest possible antiatherogenic effects of infusing Intralipid in humans.

Adenosine Diphosphate↗
PubMed1995

The association of pp125FAK, pp60Src, CDC42Hs and Rap1B with the cytoskeleton of aggregated platelets is a reversible process regulated by calcium.

The integrin alpha IIb beta 3-mediated redistribution of the tyrosine kinases pp125FAK and pp60Src and the small GTP-binding proteins CDC42Hs and Rap1B from the membrane skeleton to the cytoskeleton was found to be reversible: upon prolonged platelet aggregation (up to 15 min) induced by the thrombin-receptor activating peptide (TRAP) these signalling proteins dissociated from the cytoskeleton and reappeared in the membrane skeleton. Addition of the extracellular Ca2+ chelator EGTA and the intracellular Ca2+ chelator BAPTA/AM 30 s after TRAP allowed platelet aggregation and the association of pp125FAK, pp60Src, CDC42Hs and Rap1B with the cytoskeleton, but prevented their dissociation from the cytoskeleton. The results indicate that the prolonged elevation of cytosolic Ca2+ in stimulated platelets leads to the dissociation of signalling proteins from the cytoskeleton.

Amino Acid Sequence↗
PubMed1994

Human melanoma cell lines differ in their capacity to release ADP and aggregate platelets.

In this study we have investigated, using three different human melanoma cell lines (M1Do., M3Da., M4Be.). the varying capacity of melanoma cells to induce platelet aggregation in the presence or absence of inhibitors of ADP or thrombin. The expression levels of different integrins (alpha v, beta 3, alpha v beta 3, alpha IIb, alpha v beta 3) were evaluated by immunoprecipitation, binding and flow cytometry studies. The level of ADP in supernatants of melanoma cells were quantified by ADP bioassay and HPLC. Platelets were irreversibly aggregated by M3Da, as shown by electron microscopy, in contrast to M1Do, which induced a slow reversible aggregation. M4Be. did not induce platelet aggregation. In both cases, with M3Da. or M1Do., apyrase but not PPACK inhibited platelet induced aggregation. An anti-alpha v beta 3 monoclonal antibody (LYP18) or polyclonal antibody inhibited platelet aggregation. A similar number of LYP18 molecules bound to the surface of M1Do., M3Da. and M4Be. cell lines. Biological HPLC assays of ADP present in the supernatant of tumour cell lines showed the highest concentration of ADP to be secreted by M3Da., followed by M1Do., and none detected for M4Be. These results show that differences in in vitro aggregating potential of the three human melanoma cell lines are not related to low integrin expression levels but to their ability to generate ADP. Generation of ADP by human melanoma cells may act as important modulator of melanoma-platelet interactions.

Adenosine Diphosphate↗
PubMed1999

Pharmacological effect of nitroprusside on platelet aggregation.

Adequate platelet function and numbers are critical for postcardiopulmonary bypass patients. Endogenous and pharmacological sources of nitric oxide (NO) are known inhibitors of platelet aggregation. Sodium nitroprusside (SNP), used clinically to control blood pressure, is an inorganic source of NO. Our long-term goal is to determine if SNP infusion in the venous return line of the cardiopulmonary bypass system would preserve platelet numbers and function without affecting systemic vascular resistance. Our first requirement to accomplish this goal was to develop an assay that would detect the SNP effect on platelet aggregation. We, therefore, tested the hypothesis that clinical concentrations of SNP would inhibit platelet aggregation. We quantified platelet aggregation with the Medtronic Hepcon HMS whole blood aggregometer. Normal heparinized human blood was treated with 0.625 to 12.5 nM platelet activating factor (PAF), 0.25 to 5.0 microM epinephrine, or 0.20 to 10 microM adenosine 5'-diphosphate (ADP) to stimulate platelet aggregation. SNP was added at 10(-5) M to determine its affect on PAF, epinephrine, and ADP stimulated platelet aggregation. The results demonstrated that PAF-stimulated platelet aggregation was significantly inhibited with SNP (10(-5) M) to 82% (p < .05) of control and epinephrine and ADP mediated aggregation were not significantly affected. In conclusion, at clinically relevant concentrations SNP inhibits platelet aggregation by PAF but not with ADP or epinephrine.

Adenosine Diphosphate↗
PubMed1995

Platelet aggregability to platelet activating factor at rest and after exercise in patients with coronary artery disease.

The platelet response to the aggregatory effect of platelet-activating factor (PAF) in relation to blood PAF levels, serum PAF-acetylhydrolase (PAF-AH) activity and to their lipidaemic profile, was studied in 44 patients with coronary artery disease undergoing exercise tests. The PAF EC50 values in 21 patients with positive exercise test results were found to be significantly decreased at rest compared with 21 normal subjects (12.6 +/- 3.9 nM and 24.9 +/- 11.7 nM respectively) (P<0.0001). Moreover, the maximal percentage of aggregation to 50 nM PAF was found to be significantly increased (20.0 +/- 4.3% vs 13.5 +/- 3.6%, respectively) (P<0.0001). By contrast, the PAF EC50 values and the maximal percentage of aggregation in 23 patients with negative exercise test results were not statistically significantly different from the control group (25.2 +/- 11.4 nM and 14.1 +/- 4.7%, respectively). At the end of exercise, the PAF EC50 values and the maximal percentage of aggregation did not change in any group, and there were no significant differences in the whole-blood PAF levels either at rest or at the end of exercise. In patients with positive exercise test results, the PAF-AH activity at rest was significantly higher compared with the control group (37.2 +/- 8.0 nmol.ml(-1).min(-1) vs 32.4 nmol.ml(-1).min(-1), (P<0.03), whereas the enzyme activity did not differ in patients with negative exercise test results compared to controls (33.6 +/- 6.1 nmol.ml(-1).min(-1)). There was no change in PAF-AH activity during exercise in any group. The enzyme activity was positively correlated to the serum total and low density lipoprotein (LDL) cholesterol levels in the control group and in patients with negative exercise test results, whereas no correlation was found between PAF-AH activity and total or LDL cholesterol levels in patients with positive exercise test results.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1984

Experimental Trypanosoma cruzi cardiomyopathy in BALB/c mice. The potential role of intravascular platelet aggregation in its genesis.

In male BALB/c mice aged 5-6 weeks inoculated three times at intervals of 15 days with 1 X 10(7) epimastigote forms of the PF strain of Trypanosoma cruzi and challenged 30 days after the last inoculation with 2 X 10(4) trypomastigote forms of the Colombia strain of T cruzi (the mice were sacrificed 80-100 days after the challenge) a cardiomyopathy very similar to that observed in the chronic phase of Chagas' disease in man develops. The cardiac syndrome is characterized grossly by cardiomegaly with hypertrophy, dilatation of ventricular chambers, and thinning of the apex of the left ventricle (apical aneurysm) and microscopically by focal areas of myocytolytic necrosis and myocardial degeneration with an inflammatory response composed of mononuclear cells (predominantly macrophages and a few lymphocytes) with concurrent interstitial fibrosis and occasional myofibers containing pseudocysts. In addition, aggregated platelets and occlusive thrombi were found in small epicardial and intramyocardial vessels of infected mice as compared with controls. The potential role of intravascular platelet aggregation in the causation of focal myocardial necrosis and degeneration and apical aneurysm in experimental T cruzi cardiomyopathy in BALB/c mice is discussed.

Animals↗
PubMed1999

Increased platelet aggregability associated with platelet GPIIIa PlA2 polymorphism: the Framingham Offspring Study.

The platelet glycoprotein IIb/IIIa (GP IIb/IIIa) plays a pivotal role in platelet aggregation. Recent data suggest that the PlA2 polymorphism of GPIIIa may be associated with an increased risk for cardiovascular disease. However, it is unknown if there is any association between this polymorphism and platelet reactivity. We determined GP IIIa genotype and platelet reactivity phenotype data in 1422 subjects from the Framingham Offspring Study. Genotyping was performed using PCR-based restriction fragment length polymorphism analysis. Platelet aggregability was evaluated by the Born method. The threshold concentrations of epinephrine and ADP were determined. Allele frequencies of PlA1 and PlA2 were 0.84 and 0.16, respectively. The presence of 1 or 2 PlA2 alleles was associated with increased platelet aggregability as indicated by incrementally lower threshold concentrations for epinephrine and ADP. For epinephrine, the mean concentrations were 0.9 micromol/L (0.9 to 1.0) for homozygous PlA1, 0.7 mmol/L (0.7 to 0.9) for the heterozygous PlA1/PlA2, and 0.6 micromol/L (0.4 to 1.0) for homozygous PlA2 individuals, P=0.009. The increase in aggregability induced by epinephrine remained highly significant (P=0.007) after adjustment for covariates. For ADP-induced aggregation, the respective mean concentrations were 3.1 micromol/L (3.0 to 3.2), 3.0 micromol/L (2.9 to 3.2), and 2.8 micromol/L (2.4 to 3.3); P=0.19 after adjustment for covariates. Our findings indicate that molecular variants of the gene encoding GP IIIa play a role in platelet reactivity in vitro. Our observations are compatible with and provide an explanation for the reported association of the PlA2 allotype with increased risk for cardiovascular disease.

Adenosine Diphosphate↗
PubMed1987

Platelet aggregation increases cholinergic neurotransmission in canine airway.

To determine whether thromboxane A2 released from aggregating platelets increases the contractile response of airway smooth muscle to cholinergic nerve stimulation and, if so, what the mechanism of action is, we studied in vitro bronchial segments from dogs under isometric conditions. The contractile responses to electrical field stimulation at 30 s and 1 min after the addition of autologous platelets were increased by 11.1 +/- 3.2 (SD) and 20.7 +/- 5.4%, respectively, and were accompanied by the release of thromboxane A2. These effects were inhibited either by pretreatment of platelets with indomethacin or by addition of the thromboxane A2 receptor antagonist SQ 29548. Likewise, the thromboxane A2 mimetic U 46619, in subthreshold doses (i.e., insufficient to increase base-line tension), increased electrical field stimulation-induced contraction by 18.7 +/- 4.8%. The increase was greater in the presence of a concentration of physostigmine that did not cause spontaneous contraction and was blocked by SQ 29548 but not by hexamethonium or by phentolamine. Methacholine-induced contractions were unaffected by U 46619. These results indicate that aggregating platelets, by releasing thromboxane A2, increase the airway contractile response to neural stimulation probably by the accelerated release of acetylcholine.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2003

Cooperative effect of GNB3 825C>T and GPIIIa PI(A) polymorphisms in enhanced platelet aggregation.

INTRODUCTION: Platelet aggregation contributes to various thrombembolic disorders. Environmental factors affect platelet aggregability but only partially explain the interindividual variability in aggregation. While the platelet glycoprotein IIb/IIIa is involved in the pathogenesis of acute coronary syndromes whereas most platelet activating stimuli act via G Protein coupled receptors we investigated whether the 825C>T polymorphism of the gene GNB3 encoding the G protein beta3 subunit together with the platelet glycoprotein (GP) IIIa Pl(A) polymorphism are predictive of platelet aggregability on stimulation with various agonists acting via GPCRs. MATERIALS AND METHODS: Platelet aggregation was measured by turbidometry in 150 non-smoking individuals aged 18-40 years at a density of 2 x 10(5) platelets/microl with various agonists according to the method of Born. Genotypes of the GNB3 825C>T and glycoprotein IIb/IIIa PI(A) polymorphisms were determined using Pyrosequencing technology and restriction analysis. All functional studies were completed within 3 h. The data were analysed by Student's t-test for paired data. RESULTS: Low concentrations of agonists resulted in enhanced platelet aggregation in subjects with the GNB3 CC-genotype compared to carriers of a 825T-allele. This effect was further enhanced in carriers of the GPIIIa Pl(A2) allele (2 microM ADP: 42% vs. 19%, p=0.017; 1 microM U-46619: 51% vs. 30%, p=0.03; 5 microM epinephrine: 69% vs. 53%, p=0.025). No significant pattern of aggregation was observed on stratification by GPIIIa genotypes alone. CONCLUSIONS: Our findings indicate that two genetic markers contribute synergistically to increased platelet aggregation. This will help to identify patients at increased risk for thrombosis.

Adult↗
PubMed1983

Analysis of platelet aggregation using particle collision theory.

The aggregometer monitors changes in light transmission through stirred suspensions of aggregation platelets. Arbitrary measurements from aggregometer recorder tracings have been used to investigate platelet aggregation without regard to mechanisms involved. To determine the applicability of particle collision theory to assessment of in vitro platelet sensitivity to proaggregating agents, platelet-rich plasma (PRP) from five volunteers was used to obtain recorder tracings after addition of ADP in five doses (0.4-4.0 mumol/l PRP) to aliquots of PRP stirred and incubated in an aggregometer. Using the equation describing light transmission through particulate suspensions, particle collision theory, and s (the probability of particle union after collision), a subject- and dose-independent relationship between aggregation rate (dn/dt) and particle number (n) at the recorder tracing inflection point was found (dn/dt = -k X s X n1.56, where k is a constant dependent on particle size and speed and on the proportion of unreactive particles). Determinations of mean particle size at the tracing inflection point indicated that k was also dose independent. Dose-response curves of ADP added vs. s could therefore be constructed. This methodology provides conveniently obtainable quantitative information concerning in vitro platelet "stickiness."

Analysis of Variance↗
PubMed1992

Endothelium-derived relaxing factor inhibits thrombin-induced platelet aggregation by inhibiting platelet phospholipase C.

Endothelium-derived relaxing factor (EDRF) inhibits platelet function, but the mechanism underlying this inhibitory effect is not known. To examine this, cultured acetylsalicylic acid (ASA)-treated endothelial cells (EC) from bovine aorta (BAEC) or from human umbilical vein (HUVEC) were incubated with washed, ASA-treated human platelets. Incubation of platelets with either BAEC or HUVEC resulted in inhibition of thrombin-induced platelet aggregation that was dependent on the number of EC added. This effect was potentiated by superoxide dismutase and reversed by treating EC with NG-nitro-L-arginine or by treating platelets with methylene blue, indicating that the inhibition of platelet aggregation was due to the release of EDRF by EC. EC significantly blocked the thrombin stimulated breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the production of phosphatidic acid in [32P]orthophosphate-labeled platelets and of inositol trisphosphate in [3H]myoinositol-labeled platelets. In addition, the thrombin-mediated activation of protein kinase C (PKC) and phosphorylation of myosin light chain were inhibited in the presence of EC. Finally, thrombin stimulated an increase in cytosolic ionized calcium concentration ([Ca2+]i) in fura2-loaded platelets that was abolished by concentrations of EC which also blocked thrombin-induced aggregation. These data indicate that EDRF blocks thrombin-induced platelet aggregation by inhibiting the activation of PIP2-specific phospholipase C and thereby suppressing the consequent activation of PKC and the mobilization of [Ca2+]i.

Animals↗