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PubMed2003

Spontaneous platelet aggregation in Kawasaki disease using the particle counting method.

BACKGROUND: Platelet aggregation is generally measured by the optical density method. This method is not very sensitive in detecting platelet activation because of the poor correlation between the formation of platelet aggregates and light transmission, and inability to detect small platelet aggregates. Recently, a new method was developed that detects small platelet aggregates formed in the early phase of platelet aggregation by means of a particle counting technique using light scattering. METHODS: The present study used the particle counting method to measure spontaneous platelet aggregation (SPA) produced by agitation with a stirrer bar without agonists in patients with Kawasaki disease (KD) and children's thrombotic disease, and compared the results with the conventional optical density method. RESULTS: Using the particle counting method, significantly higher SPA rates were found before treatment than in healthy adults and at the other stages of treatment. A similar tendency was noted with the optical density method; however, the positive rate of SPA was significantly higher with the particle counting method in each stage except the second stage, which was the period from the start of gamma-globulin therapy to 20 days. CONCLUSION: These results indicate that enhanced platelet aggregation is noted at a high frequency before treatment of KD and that the particle counting method is superior to the optical density method in detecting enhanced platelet aggregation.

Adult↗

PubMed1983

Mepacrine blockade of arachidonate-induced washed platelet aggregation: relationship to mepacrine inhibition of platelet cyclooxygenase.

Mepacrine, in addition to its established antilipolytic activity, was also found to inhibit the conversion of 14C-arachidonic acid to 14C-thromboxane B2 in human washed platelets. In the concentration range of 3.33-33 microM, meparcrine exerted a dose dependent inhibition of arachidonate conversion to thromboxane B2 in parallel to inhibition of arachidonate-induced platelet aggregation. Mepacrine inhibition of thromboxane formation was not accompanied by a concomitant increase in other cyclooxygenase products. Furthermore, mepacrine did not affect platelet transformation of added prostaglandin H2 to thromboxane A2 and other products. These results indicate that mepacrine inhibits the cyclooxygenase enzyme and not thromboxane synthase. In washed platelets, mepacrine inhibition of arachidonic acid conversion to thromboxane A2 appears to be a major factor in the overall inhibitory effect of the compound on the combined process of arachidonate release from cellular phospholipids and its conversion to proaggregatory products.

Arachidonic Acid↗

PubMed1985

Effects of dipyridamole on the glyceryl-trinitrate-induced inhibition of coronary artery muscle tone and platelet aggregation in relation to cyclic nucleotide metabolism.

The effects of glyceryl-trinitrate (GTN) and dipyridamole (DIP) on relaxation of bovine coronary arteries and on inhibition of aggregation of human platelets have been studied in vitro with special reference to the cyclic GMP (cGMP) system. GTN had a dose-dependent relaxant effect on bovine coronary arteries, and at a high concentration (10(-5) M) it had an inhibiting effect on platelet aggregation. The effects were associated with an increase in the cGMP levels of the tissues. DIP (5 X 10(-7) M respectively 5 X 10(-6) M) potentiated the coronary artery relaxation induced by GTN (10(-8) M) and the inhibition of platelet aggregation caused by GTN in the concentrations 10(-7)-10(-4) M. The potentiation was associated with higher levels of cGMP than those produced by GTN alone, at least in bovine coronary arteries. However, at a concentration of 10(-4) M, GTN, in combination with DIP, caused a significant fall in the cGMP level compared to GTN alone. GTN and DIP were not found to significantly increase the cAMP levels in the concentrations tested. DIP was shown to inhibit phosphodiesterase (PDE) from both platelets and bovine coronary arteries. This might be one of the possible mechanisms that can explain the above mentioned potentiation. It is suggested that the combination of DIP + GTN may be of some clinical importance since the potentiating effects were seen at concentrations comparable to the therapeutic plasma concentration for the respective drugs.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed1992

1,5-Benzodiazepines. X. Dialkylamino substituted 1,5-benzodiazepine and [1,2,4]triazolo [4,3-a][1,5] benzodiazepine derivatives with inhibitory activity on PAF-induced platelet aggregation.

Novel 4-(dialkylamino) substituted (4, 5 c, 8) and 2,4-bis(dialkylamino) substituted (6) 1,5-benzodiazepine derivatives were synthesized. Both these new compounds and the substituted 4H-[1,2,4]triazolo[4,3-a][1,5]benzodiazepine-5-amines 2 a-h, recently described by us, were tested in vitro for their inhibitory activity on the PAF-induced aggregation of human platelets. Actually, bicyclic compounds 4 d, 5 c and tricyclic compounds 2 g, h showed a significant activity: in all them the dialkylamino substituent was the 4-(ethoxycarbonyl)-1-piperazinyl group. On the contrary, compounds 4 d, 5 c, 2 g,h showed practically no inhibitory activity when platelet aggregation was induced by ADP, A23187, or collagen.

Benzodiazepines↗

PubMed1986

Comparison of the inhibitory effects of aspirin and ticlopidine on platelet aggregation and Ca2+ mobilization in rat platelets.

To study the cause of the sex difference in the inhibitory effects of aspirin on platelet functions, we compared the effects of aspirin and ticlopidine in rat platelets. Aspirin showed the sex difference in the effects on the collagen-induced platelet aggregation and the malondialdehyde (MDA) production, but ticlopidine showed no sex difference in the effects on those. The C-AMP level in male rat platelets was the same as that in female rat platelets. Ticlopidine increased the C-AMP level in rat platelets, but aspirin did not. Aspirin suppressed the intracellular Ca2+ mobilization in male rat platelets more strongly than in female rat platelets. Ticlopidine suppressed the Ca2+ mobilization in both sexes equivalently. The above results suggest that the sex difference in the inhibitory effects of aspirin on rat platelet functions comes from the sex difference in the thromboxane (TX) production in rat platelets.

Animals↗

PubMed1995

Flavocetin-A and -B, two high molecular mass glycoprotein Ib binding proteins with high affinity purified from Trimeresurus flavoviridis venom, inhibit platelet aggregation at high shear stress.

Two high molecular mass proteins, flavocetin-A and flavocetin-B, were purified from Trimeresurus flavoviridis venom. On polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate, the apparent molecular mass of flavocetin-A and -B were 149 and 139 kDa, respectively, under nonreducing conditions. On reduction, flavocetin-A showed two distinct subunits (17 and 14 kDa), and flavocetin-B three distinct subunits (17, 15 and 14 kDa). At 1 microgram/ml, flavocetin-A and -B (flavocetins) inhibited the von Willebrand factor (vWF)-dependent aggregation of fixed human platelets. However, flavocetins (10 micrograms/ml) had no effect on ADP- and collagen-induced platelet aggregation in PRP. Flavocetins (3 micrograms/ml) also inhibited shear-induced platelet aggregation at high shear stress. Furthermore, flavocetin-A completely inhibited the aggregation of and ATP release from washed platelets stimulated with a low concentration of thrombin. Flavocetin-A specifically bound to platelet with high affinity (Kd = 0.35 +/- 0.13 nM) at 21,500 +/- 1760 binding sites per platelet. The N-terminal amino acid sequences of the subunits of flavocetin-A show a high degree of homology with those of echicetin, botrocetin, alboaggregin-B and factor IX/factor X-binding protein. These results suggest that flavocetins may be a useful tool for further investigation of the GPIb-vWF interaction.

Adenosine Triphosphate↗

PubMed1998

[Effects of lotensin and nitrendipine on plasma fibrinogen and platelet aggregation in hypertensive patients].

Plasma fibrinogen and platelet aggregation were measured by turbidimetric immunoassay, turbidimetry in 47 hypertensive patients and 20 normotensive control subjects. Among the 47 hypertensives, 24 cases were received lotensin and 23 nitrendipine. The plasma fibrinogen was increased and platelet aggregation enhanced in hypertensive patients before treatment. Platelet aggregation decreased after 8 weeks of treatment with lotensin or nitrendipine respectively. Lotensin decreased plasma fibrinogen whereas nitrendipine did not. It was concluded that both lotensin and nitrendipine decreased platelet aggregation; lotensin decreased plasma fibrinogen but nitrendipine did not.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1989

A compartmental model of platelet aggregation in vitro: the kinetics of single platelets.

A compartmental model of platelet aggregation which accurately describes both reversible and irreversible aggregation in vitro is presented. This model is substantiated by correlative analyses of agonist-induced aggregation as monitored by both routine aggregometry and resistive counting of single platelets. Previously unresolved differences in the reported reaction order of the aggregation process are explained. The model suggests that aggregation includes, in addition to the association and dissociation of platelets, the stabilization of aggregates. We find reversible aggregation requires that single platelets associate more rapidly than aggregates stabilize. For irreversible aggregation, our results suggest the presence of subpopulations of single platelets which associate at different rates. As an unexpected consequence of this study, quantitative relationships between photometric and resistive methods of monitoring platelet aggregation are elucidated.

Adenosine Diphosphate↗

PubMed1983

The effect of low-dose aspirin and platelet aggregation in familial hypercholesterolaemia.

Since the platelets of patients with familial hypercholesterolaemia (FH) are hyperaggregable, the inhibitory effect of low-dose aspirin on platelet aggregation in response to adenosine diphosphate, collagen, adrenaline and arachidonic acid was tested in 9 young adult patients with FH and compared with that in 9 normal subjects. After a single oral dose (150 mg) of aspirin the degree of inhibition of platelet aggregation was the same in the two groups, as was the recovery time (in days) for full restoration of platelet aggregation . In a second experiment in which 162 mg aspirin was administered daily for 28 days, inhibition of platelet aggregation was sustainable in both the patient and the control groups. These results suggest that despite the recognized hyperaggregability of platelets from patients with FH, daily low-dose aspirin ingestion effectively inhibits their in vitro aggregation and may therefore prove beneficial as supplemental therapy to reduce the rate of myocardial infarction in this high-risk group.

Adult↗

PubMed1982

Abnormal platelet aggregation response in Huntington's disease.

Platelet aggregation response to epinephrine, dopamine, serotonin, adenosine diphosphate, arachidonic acid, and collagen was examined in seven patients with Huntington's disease and nine of their relatives. All patients, except for two cases that were in terminal states, showed enhanced response to all the stimulants, especially to dopamine and epinephrine. The platelet aggregation response in many relatives also deviated from the normal limit. The relationship between platelet aggregation abnormality in Huntington's disease and the pathophysiology of the disease was discussed from the view of a generalized membrane defect hypothesis in Huntington's disease, and of disturbed cathecholamine metabolism, both in the CNS and periphery. A possibility that platelet aggregation response examination will be a useful screening test of offspring at risk was proposed.

Adenosine Diphosphate↗

PubMed1978

Release of prostaglandin-like substances and lung reactions to induced intravascular platelet aggregation in cats.

Induced intravascular aggregation of blood platelets gives pulmonary vasoconstrictor and bronchoconstrictor responses, which might be mediated by bioactive substances from the platelets. The aim of the present work was to see if these lung reactions could be related to the release of prostaglandin-like substances (PGLS). Repeated episodes of platelet aggregation were induced by i.v. infusions of collagen in anaesthetized cats ventilated at a constant tidal volume. Arterial blood was pumped from a carotid artery (10 ml/min) to superfuse a series of smooth muscle organs sensitive to prostaglandins (PGs): rabbit aorta, rat stomach strip, rat colon and chick rectum. In two experiments cat jejunum replaced the rabbit aorta in order to detect kinins. All tissues were pretreated with antagonists against catecholamines, histamine, serotonin and acetylcholine. The bioassay tissues were calibrated with standard doses of PGE2 and PGF2alpha. Collagen infusions caused lung responses (as judged from the rise in peak tracheal pressure) and in most cases also a transient systemic hypotension. Simultaneously, contractions of the bioassay tissues occurred, indicating release of PGLS. Such release was only detected as long as lung responses could be elicited by i.v. collagen infusions. These findings imply that PGs and/or the various intermediates in PG synthesis might mediate the pulmonary smooth muscle constriction occurring after intravascular platelet aggregation.

Angiotensin II↗

PubMed1992

Nitric oxide and prostacyclin inhibit fetal platelet aggregation: a response similar to that observed in adults.

OBJECTIVE: We evaluated the relative importance of two endothelium-derived substances, prostacyclin and nitric oxide, in their ability to inhibit aggregation of fetal and maternal platelets. STUDY DESIGN: The effects of various concentrations of prostacyclin and S-nitroso-N-acetylpenicillamine (which releases nitric oxide) on platelet aggregation were studied by means of platelet-rich plasma from at least five to six subjects per group. Fetal blood was collected from umbilical vein at delivery. Maternal venous blood was collected within 4 hours of delivery. Platelet aggregation was monitored with a platelet aggregation profiler. Adenosine diphosphate was used as the aggregating agent. Statistical differences between means were evaluated with two-way analysis of variance or Student t test. RESULTS: Prostacyclin and S-nitroso-N-acetylpenicillamine inhibited aggregation of fetal and maternal platelets, but prostacyclin was more potent. Fetal platelets were more sensitive than maternal platelets to prostacyclin and S-nitroso-N-acetylpenicillamine. CONCLUSION: Prostacyclin appears to be more important in preventing aggregation of platelets in the feto placental circulation.

Adenosine Diphosphate↗

PubMed1996

Direct inhibitory mechanisms of halothane on human platelet aggregation.

BACKGROUND: Although halothane directly inhibits platelet aggregation, the mechanisms of this effect are still unknown. The current study aimed to clarify the inhibitory mechanisms of halothane on thrombin-induced human platelet aggregation by measuring (1) platelet-surface glycoprotein Ib expression, (2) the concentration of intracellular free Ca2+ ([Ca2+]i) measured simultaneously with aggregation, (3) the concentration of intracellular inositol 1,4,5-triphosphate, and (4) the concentration of intracellular cyclic 3',5'-adenosine monophosphate ([cAMP]i). METHODS: Washed platelet suspensions, obtained from healthy volunteers, were preincubated with halothane (0-2 mM) for 2 min and then exposed to 0.02 units/ml thrombin for 3 min. The glycoprotein Ib bound to fluorescein-labeled antibody was measured by fluorescence flow cytometry. [Ca2+]i was measured, simultaneously with aggregation, in Fura-2 (Ca2+ indicator)-loaded platelets by use of a fluorometer. Inositol 1,4,5-triphosphate and [cAMP]i were measured by radioimmunoassay. RESULTS: Halothane had no effect on glycoprotein Ib expression with or without thrombin. Halothane decreased the thrombin stimulated [Ca2+]i transient and inhibited platelet aggregation in a dose-dependent manner, both in the presence and in the absence of external Ca2+. Isoflurane had no apparent effect on either platelet aggregation or [Ca2+]i in the absence of external Ca2+. Halothane inhibited the increase in inositol 1,4,5-triphosphate induced by thrombin. Halothane moderately but significantly increased [cAMP]i, but the adenylate cyclase activator forskolin (which has the same inhibitory ability on aggregation as halothane) increased [cAMP]i to a much greater extent than did halothane. CONCLUSIONS: Halothane inhibits thrombin-induced human platelet aggregation by decreasing [Ca2+]i without inhibiting agonist-receptor binding; the inhibitory effect of halothane on [Ca2+]i might be mediated by a decrease in inositol 1,4,5 triphosphate and in part by an increase in [cAMP]i.

Adult↗

PubMed1989

Interaction between SIN-1 and prostacyclin in inhibiting platelet aggregation.

SIN-1, the metabolite of molsidomine, caused a dose-dependent inhibition of the aggregation of rabbit platelets induced by adenosine diphosphate (ADP) and the stable thromboxane mimetic U-46619. Molsidomine was inactive in this respect. In the presence of a threshold concentration of prostacyclin, the antiaggregating activity of SIN-1 became more pronounced. As a result, the dose-response curve of SIN-1 was shifted to the left. These findings suggest that SIN-1 could be of therapeutic value to suppress platelet aggregation during atherosclerotic disease when the endogenous supply of endothelium-derived relaxing factor is compromised.

Animals↗

PubMed1984

Mechanism of action of the platelet aggregation inhibitor purified from Agkistrodon halys (mamushi) snake venom.

The platelet aggregation inhibitor purified from Agkistrodon halys snake venom inhibited rabbit platelet aggregations induced by thrombin, sodium arachidonate, collagen or ionophore A-23187. The IC50 was about 11 micrograms/ml in platelet aggregation regardless of which aggregation inducer was used. beta-Mercaptoethanol abolished both the phospholipase A enzymatic and platelet aggregation inhibitory activities of this venom inhibitor. p-Bromophenacyl bromide-treated venom inhibitor lost almost completely its phosphilipase A enzymatic activity, but retained its platelet aggregation inhibitory effect. In the presence of EGTA, the venom inhibitor still showed the same inhibitory activity on thrombin-, sodium arachidonate-, collagen- or ionophore A23187-induced platelet aggregations triggered by successive addition of Ca2+. The activation of platelet phospholipase A and the serotonin release reaction triggered by Ca2+ influx were unaffected by this venom inhibitor. It also inhibited the clot retraction of platelet-rich plasma. It is concluded that the inhibitory effect of the venom inhibitor on platelet aggregation is independent of its phospholipase A enzymatic activity. Its mode of action is different from those of other known platelet inhibitory drugs. This venom inhibitor possibly acts on a common step subsequent to platelet shape change, leading to inhibition of platelet aggregation.

Animals↗

PubMed1994

Platelet activation by platelet aggregation factor from Eisenia foelide.

A platelet activating factor from earthworm, Eisenia foelide (EPAF, 25.9 mumol.L-1), induced human platelet aggregation and 5-HT (maximal release of 89% at EPAF 74.1 mumol.L-1) was detected during this process. Neither creatine phosphate/creatine phosphate kinase (CP/CPK) nor aspirin completely inhibited the EPAF-induced platelet aggregation. In the presence of fibrinogen, EPAF (55.6 mumol.L-1) induced the aggregation of human platelet which had been thrombin-treated and degranulated. Results indicated that EPAF was a potent platelet agonist and the EPAF-induced platelet aggregation was ADP- and TXA2-independent.

Animals↗

PubMed1983

Platelet aggregation response in schizophrenia and prostaglandin E1.

Platelet aggregation response to various stimulants was examined in 18 unmedicated schizophrenic patients, 13 medicated patients, and 13 control subjects. Platelet aggregation response to epinephrine decreased only in unmedicated schizophrenic patients. Clinical improvement in seven patients after neuroleptic medication was significantly correlated with an increase in platelet aggregation response to arachidonic acid, and nonsignificantly to epinephrine, dopamine, and serotonin. The inhibitory effect of prostaglandin E1 on platelet aggregation response to adenosine diphosphate was investigated in seven unmedicated schizophrenic patients, six medicated patients, and eight controls. The inhibitory effect of prostaglandin E1 on platelet aggregation response to adenosine diphosphate was significantly reduced in all unmedicated schizophrenic patients. Neuroleptic medication had some effect in normalizing aberrant sensitivity to prostaglandin E1 in those patients, although acute medication induced an adverse reaction in the controls.

Adenosine Diphosphate↗

PubMedDate not supplied

Influence of dehydroepiandrosterone on platelet aggregation, superoxide dismutase activity and serum lipid peroxide concentrations in rabbits with induced hypercholesterolemia.

UNLABELLED: Special interest in the role of DHEA dates back to the finding of a correlation between low serum DHEA concentrations and a higher morbidity and mortality rate due to coronary diseases in humans. Animal studies with experimental atherosclerosis confirmed the anti-sclerotic effect of DHEA. The mechanism of DHEA action remains unclear. We determined the influence of dehydroepiandrosterone (DHEA) administration, a potential anti-atherogenic agent, on platelet aggregation, platelet superoxide dismutase (SOD) activity and serum lipid peroxide (LPO) levels in male rabbits fed on a normal and atherogenic diet. 44 adult male New Zealand white rabbits were divided into 4 groups: 1--control group fed on standard rabbit food, 2--fed on an atherogenic diet, 3--fed on an atherogenic diet with DHEA, 4--fed on standard food with DHEA. We detected blood platelet aggregation following (ADP) and collagen activation by means of photometry. Platelet SOD activity was detected by means of fluorometry determining the inhibition of adrenaline auto-oxidation. The serum LPO concentration was measured by means of the colorimetric method. The serum DHEA-S concentration was measured by means of RIA methods, and serum lipid levels were measured by means of Biomérieux manufactured kits. Results demonstrate that (1) elevated LPO concentrations in rabbits with hyperlipidemia did not decrease following DHEA administration. (2) In rabbits fed on a normal diet, DHEA caused a decrease of LPO, which emphasizes the positive influence of this steroid on the oxidative stress in healthy animals. Such a result was not seen in the group with severe hyperlipidemia. (3) Rabbits with hyperlipidemia demonstrated a significantly decreased SOD activity. (4) In healthy animals as well as in those with hyperlipidemia, DHEA administration caused an increase of platelet SOD activity, the main enzyme of the antioxidant defence system, which protects the organism against free radical damage (5) (DHEA had no influence on platelets aggregation in both tested groups). IN CONCLUSION: DHEA administration improves platelet SOD activity, which protects cells against oxidative damage. The hypothesis that DHEA administration leads to an increase in antioxidant potency requires further investigations.

Adenosine Diphosphate↗