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PubMedDate not supplied

Adenosine diphosphate-induced platelet aggregation in the states of hypercoagulability.

One hundred and seven patients with congestive heart failure, myocardial infarction and arteriosclerotic heart disease were studied by adenosine diphosphate-induced platelet aggregation, fibrinogen levels and ethanol gelation test. Both increases and decreases in platelet aggregation were observed. A significantly high percentage of patients showed a decreased platelet aggregation which was especially marked in the more acute as opposed to the less acute phase. In addition, most patients exhibited a marked shift from abnormal to normal platelet aggregation or vise-versa within a short time period. This pattern of platelet aggregation suggests an active role of platelets in the states of hypercoagulability. The hypercoagulability of these patients was further substantiated by a high percentage of positive ethanol gelation tests and high fibrinogen levels.

Adenosine Diphosphate↗
PubMed1983

Isolation and partial characterization of platelet aggregation inhibitors in the blood of dialyzed patients.

Platelet aggregation inhibitors were isolated from the blood of dialyzed patients by high-performance liquid chromatography. At least two inhibitors exist in the blood of dialyzed patients. These inhibitors not only inhibit platelet aggregation, but also suppress the chemiluminescence response of platelet. The chromatographic behaviors and the results of enzymatic digestion suggested that these inhibitors are relatively low molecular weight nonpeptidic substances.

Blood Platelets↗
PubMed1984

The kinetics of platelet aggregation induced by fluid-shearing stress.

The work herein examines in vitro the kinetics of platelet aggregation in response to the fluid-shearing stress imparted by a rotational viscometer. Aggregation is expressed through changes in particle size histograms and total particle count. Platelet aggregation commenced above 2000 sec-1 shear rate and was stable above 5000 sec-1. Activation by shear required less than 10 sec at all shear rates. At shear rates above 5000 sec-1, the particle count fell by one-half within 10 sec. By this point aggregates of 1000 platelets or more had appeared. Diluting the platelet suspensions suppressed shear-induced aggregation but not aggregation to ADP, supporting the hypothesis that shear-induced platelet aggregation proceeds through chemical release.

Adult↗
PubMed1985

Effect of Iloprost (ZK 36 374), a novel prostacyclin analogue, on ADP-induced platelet aggregation.

The effect of Iloprost (ZK 36 374), a chemically stable carboprostacyclin derivative, on ADP-induced platelet aggregation was investigated using platelet-rich plasma obtained from healthy male volunteers. It was shown that Iloprost in a dose-dependent fashion powerfully inhibits both the primary and secondary wave of ADP-induced platelet aggregation. Similarly, Iloprost immediately and most effectively disaggregates preformed platelet aggregates.

Adenosine Diphosphate↗
PubMed1977

Intravascular platelet aggregation and acute respiratory insufficiency.

Respiratory effects of long-lasting episodes of intravascular platelet aggregation have been studied in cats. Animals in 1 group had the chest opened and were given mechanical ventilation with a constant tidal volume. Animals of another group were breathing spontaneously. Platelet aggregation was induced by intravenous infusion (for 1 hr) of a suspension of collagen fibrils. Such infusions caused acute respiratory distress in both groups. Severe arterial hypoxemia and rapid breathing as well as constriction of airways and lung vessels occurred. Most of these changes were reversed within 2 hr after collagen infusion had ended. Deep lung inflations markedly improved lung function. It is concluded that an acute, but reversible pulmonary insufficiency might be caused by pulmonary microembolization due to intravascular platelet aggregation. The arterial hypoxemia is suggested to be caused by disturbances in the ventilation-perfusion ratio secondary to airway constriction and closure. The present findings also imply that besides platelet aggregation, some additional factors are necessary for irreversible or progressive respiratory insufficiency to develop.

Animals↗
PubMed1992

Effect of synthetic enantiomeric cannabinoids on platelet aggregation.

The effect of a synthetic pair of enantiomeric cannabinoids on platelet function was evaluated. The nonpsychotropic enantiomer, the 1,1-dimethylheptyl homolog of (+)-(3S,4S)-7-hydroxy-delta-6-tetrahydrocannabinol (HU-211), was found to be more active in inhibiting ADP-induced platelet aggregation than the highly psychotropic (-)-enantiomer (HU-210). The related (+)-(3R,4R) cannabinoid, HU-213, which lacks the 7-hydroxy moiety, exerted its inhibitory effect within a wider range of concentrations. The results indicate a differentiation between psychotropic activity and inhibition of platelet aggregation in the cannabinoid group of compounds.

Adenosine Diphosphate↗
PubMed1999

Rhodocetin, a novel platelet aggregation inhibitor from the venom of Calloselasma rhodostoma (Malayan pit viper): synergistic and noncovalent interaction between its subunits.

A novel platelet aggregation inhibitor, rhodocetin, was purified from the crude venom of Calloselasma rhodostoma. It inhibited collagen-induced platelet aggregation in a dose-dependent manner, with an IC50 of 41 nM. Rhodocetin has a heterodimeric structure with alpha and beta subunits, which could be separated on a nonreducing denaturing gel or reverse-phase HPLC column. Individually neither subunit inhibited platelet aggregation even at 2.0 microM concentration. Titration and reconstitution experiments showed that, when these subunits are mixed to give a 1:1 complex, most of its biological activity was recovered. The reconstituted complex inhibited platelet aggregation with an IC50 of 112 nM, about 3-fold less effective than the native molecule. Circular dichroism analysis revealed that the reconstituted complex had a spectrum similar to that of the native protein. By using surface plasmon resonance studies, we established that the stoichiometry of binding between the two subunits is 1:1 and the subunits interact with a Kd of 0.14 +/- 0.04 microM. The complete amino acid sequences of the alpha (15956.16 Da, 133 residues) and beta (15185.10 Da, 129 residues) subunits show a high degree of homology with each other (49%) and with the Ca2+-dependent lectin-related proteins (CLPs) (typically 29-48%) isolated from other snake venoms. Unlike the other members of the family in which the subunits are held together by an interchain disulfide bond, rhodocetin subunits are held together only through noncovalent interactions. The cysteinyl residues forming the intersubunit disulfide bridge in all other known CLPs are replaced by Ser-79 and Arg-75 in the alpha and beta subunits of rhodocetin, respectively. These studies support the noncovalent and synergistic interactions between the two subunits of rhodocetin. This is the first reported CLP dimer with such a novel heterodimeric structure.

Amino Acid Sequence↗
PubMed1989

Platelet aggregability after endoscopic intravariceal injection of 5 per cent ethanolamine oleate into oesophageal varices.

Platelet aggregability and the coagulative and fibrinolytic systems were examined in 45 patients who underwent endoscopic injection sclerotherapy for oesophageal varices. Five per cent ethanolamine oleate, the sclerosant used, was injected into the oesophageal varices. There were significant increases in the concentrations of fibrinopeptide A, fibrinopeptide B-beta-15-42 and fibrin degradation products-E after the sclero-therapy. At 1 h after the sclerotherapy the mean(s.e.m.) platelet aggregation was significantly suppressed to 71.9(4.2) per cent of that before the treatment (P less than 0.01). There was a gradual recovery within 1 week to the same level seen before the sclerotherapy. Thromboxane B2 and 6-keto-prostaglandin F1 alpha, both stable products of thromboxane A2 and prostacyclin respectively, showed significant temporary increases after the sclerotherapy (P less than 0.01). The peak increase in the level of thromboxane B2 was noted within 1 h after the sclerotherapy and earlier than that for 6-keto-prostaglandin F1 alpha. This increased ratio of prostacyclin and thromboxane A2 may be related to the marked limitation in platelet aggregation.

6-Ketoprostaglandin F1 alpha↗
PubMed1975

Inhibition of platelet aggregation caused by estrogen treatment in patients with carcinoma of the prostate.

Platelet aggregation is increased in patients with carcinoma of the prostate treated with estrogens. Hence, these patients have a high incidence of cardiovascular and thromboembolic diseases. Platelet aggregation has been tested with the platelet aggregation test. It was inhibited by administration of 500 mg. acetylsalicylic acid twice daily. An aggregation inhibiting effect has been found in all 38 patients. To reduce the excess hazards of cardiovascular complications of estrogens in treating carcinoma of the prostate acetylsalicylic acid is recommended as an adjunct therapy.

Aspirin↗
PubMed1989

[Effect of a new thromboxane A2 antagonist, S-145, on platelet aggregation].

The newly synthesized compound S-145, (+/-)-5(Z)-7-(3-endo-phenylsulfonylamino [2.2.1] bicyclohept-2-exo-yl)heptenoic acid, inhibited arachidonic acid (AA)-, 9,11-methanoepoxy-PGH2 (U46619)-, collagen- and ADP-induced human platelet aggregation in vitro with IC50 values of 0.25, 0.34, 0.22, and 0.08 microM, respectively. The inhibiting potency of this compound to AA- or U46619-induced platelet aggregation was about twice that of ONO-3708 and 1/7-1/14 that of SQ29,548 in human platelets, about 7 times that of ONO-3708 and 1/3-1/7 that of SQ29,548 in guinea pig platelets, and 250-800 times that of ONO-3708 and 1-7 times that of SQ29,548 in rabbit platelets. When S-145 was administered orally to guinea pigs at the dose of 0.1 mg/kg, AA-induced platelet aggregation was completely inhibited at 30 and 60 min after the administration, but not at 3 and 6 hr. The minimum effective doses of S-145 (p.o.) to AA- and collagen-induced platelet aggregation at 60 min after the administration were 0.01 mg/kg and 0.03 mg/kg, respectively. The potency of S-145 (p.o.) to inhibit AA- and collagen-induced guinea pig platelet aggregation was 30-300 times that of ONO-3708 or SQ29,548 and 300-1000 times that of aspirin. These results suggest that S-145 is a thromboxane A2 antagonist showing a potent inhibiting effect on platelet aggregation by oral administration.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1999

Effects of dietary n-3 polyunsaturated fatty acids from plant and marine origin on platelet aggregation in healthy elderly subjects.

In the present intervention study we compared the effects of alpha-linolenic acid with those of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on platelet aggregation in vitro and ex vivo in healthy non-institutionalized elderly subjects. We also compared the effects of alpha-linolenic acid on platelet aggregation in elderly subjects with those in younger volunteers. During a run-in period of 3 weeks all subjects (thirty-eight elderly (> 60 years) and twelve younger volunteers (< 35 years)) received a diet rich in oleic acid. For the next 6 weeks the elderly subjects received a diet rich in oleic acid (n 11), alpha-linolenic acid (n 14) (6.8 g/d) or EPA/DHA (n 13) (1.05 g EPA plus 0.55 g DHA). The younger subjects were given a diet rich in alpha-linolenic acid. The diets did not affect ADP- or collagen-induced platelet aggregation in vitro in either platelet-rich plasma or whole blood. The ex vivo platelet aggregation as measured with filtragometry was significantly decreased in the elderly group that received EPA/DHA compared with the alpha-linolenic acid (P = 0.006) and the oleic acid (P = 0.005) diet groups. Effects of alpha-linolenic acid were not age-dependent. Our results suggest that alpha-linolenic acid and EPA/DHA do not change in vitro platelet aggregation. Compared with oleic acid, EPA/DHA, but not alpha-linolenic acid, favourably affects ex vivo platelet aggregation in healthy elderly subjects.

Adolescent↗
PubMed2005

Effects of physiological leptin administration on markers of inflammation, platelet activation, and platelet aggregation during caloric deprivation.

CONTEXT: Leptin is a nutritionally regulated adipocyte-derived cytokine. Previous studies in obese patients have demonstrated increased inflammatory markers and increased platelet aggregation in association with leptin. However, the effects of leptin administration on markers of inflammation and platelet aggregation in a human model of undernutrition have not previously been studied. OBJECTIVE: The objective of the study was to investigate markers of inflammation, platelet activation, and platelet aggregation in a model of caloric deprivation and increased leptin sensitivity. DESIGN: This study was a randomized, placebo-controlled study conducted between November 2002 and November 2003. SETTING: The study was conducted at an inpatient care setting at the General Clinical Research Center. PARTICIPANTS: Twenty healthy, young (18-35 yr old), normal-weight (body mass index, 20-26 kg/m2) women were recruited from local advertisements. No subjects withdrew due to adverse effects. INTERVENTION: The effects of physiological recombinant methionyl human leptin or identical placebo administration were investigated over a 4-d fast. MAIN OUTCOME MEASURES: The primary outcome measures for this study were C-reactive protein (CRP) and indices of platelet activity. RESULTS: Leptin administration prevented the fasting-induced decline in leptin (P < 0.05 vs. placebo at each time point). Leptin administration increased CRP (6.3 +/- 2.4 vs. 0.7 +/- 0.3 mg/liter; P = 0.04), circulating P-selectin (11.6 +/- 10.2 vs. -28.9 +/- 15.6 ng/ml; P = 0.04), and induction of platelet aggregation (5.8 +/- 2.6 vs. -2.7 +/- 2.9%, P = 0.04, percent maximum platelet aggregation) relative to placebo administration (change in leptin vs. change in placebo, respectively, for each variable). Leptin tended to increase serum amyloid A [0.1 +/- 0.2 vs. -0.3 +/- 0.1 log10 (ng/ml); P = 0.07], and the changes in serum amyloid A and CRP were highly correlated (r = 0.83; P < 0.0001). No changes in TNFalpha, IL-6, IL-10, plasminogen activator inhibitor-1, haptoglobin, intercellular adhesion molecule, or vascular cell adhesion molecule were seen between the groups. CONCLUSIONS: Our data provide evidence that physiological leptin administration stimulates inflammatory and platelet responses in humans during caloric deprivation.

Adult↗
PubMed1996

Effects of moderate consumption of red wine on platelet aggregation and haemostatic variables in healthy volunteers.

OBJECTIVE: To evaluate the effect of moderate consumption of red wine on platelet aggregation and haemostatic variables, discriminating the effect of alcohol from that of non-alcoholic components. DESIGN: A randomised crossover study. SETTING: The Department of Food Science and Technology, University of Milan. SUBJECTS: Eleven healthy male volunteers who were moderate drinkers. INTERVENTIONS: For three periods of four weeks, subjects drank three different beverages [320 ml of red wine (providing 30 g/day of alcohol), 30 g/day of alcohol diluted in 320 ml of clear fruit juice or 320 ml of dealcoholised red wine] during the two main meals. Each treatment was preceded by a period of four weeks of complete withdrawal from any alcoholic beverage. At the end of each period platelet aggregation after collagen and ADP stimulus, and levels of fibrinogen, plasminogen, tissue-type plasminogen activator (t-PA) antigen and von Willebrand factor (vWF) were determined. RESULTS: Consumption for a period of four weeks of 30 g/day of alcohol either from red wine or alcohol resulted in similar decreases of collagen-induced platelet aggregation and fibrinogen levels. ADP-induced platelet aggregation, t-PA antigen, vWF and plasminogen levels were not affected by any treatment. No differences were detected when we compared platelet function and the other haemostatic variables at the end of red wine and dealcoholised treatments with findings at the end of alcohol treatment and abstinence. CONCLUSIONS: The well known positive effect of moderate consumption of red wine on haemostasis seems due to alcohol and not to the non-alcoholic fraction present in red wine.

Adenosine Diphosphate↗
PubMed2000

[Morning rise of systolic blood pressure (by 24-hour ambulatory monitoring) and platelet aggregability in essential hypertension patients].

AIM: To investigate the relationship between platelet aggregability (PA) and parameters of blood pressure (BP) in patients with essential hypertension (EH). MATERIALS AND METHODS: We analyzed 24-h BP recordings (SL-90207, 15-min day and 30 min night time intervals) of 47 hospitalized males with mild to moderate EH (mean age 48 +/- 1 years) to assess the following parameters: mean 24-h, awake (Aw) and nighttime (N) systolic (S) and diastolic (D) BP. We assessed the morning rise (MR) of BP using the new index: a relative morning rise of systolic BP-RMRSBP--(max value of SBP from 6 am to 12 am/mean asleep SBP) x 100%. The kinetics of mean aggregate size (MAS) changes was studied with aggregation analyzer model (230LA Biola Ltd., Russia). The following parameters were used for estimation of platelet aggregability: a relative increase in MAS 2 min after beginning of sample stirring--for spontaneous aggregation (SPA) and the maximum increase in the light transmission for 0.5 microM ADP-induced aggregation (ADPI-PA). The patients were divided into two groups according to the median value of RMRSBP: group 1 (n = 25, RMRSBP < 121%) and group 2 (n = 22, RMRSBP > 121%). The differences in estimated parameters were tested by Student two tailed t-tests and presented by M +/- SE. P < 0.05 was considered statistically significant. RESULTS: No significant differences have been found between the groups by mean age, body mass index, duration of arterial hypertension, mean 24-h, awake DBP and SBP. Statistically significant differences have been found between groups by SPA, ADPI-PA, night SBP, night DBP, RMRSBP, RMRDBP. In group 2 there was a correlation between RMRSBP and SPA, but not in group 1. CONCLUSIONS: The morning rise of systolic BP is associated with an increase of ADP-induced and spontaneous platelet aggregability in the patients with mild to moderate essential hypertension and apparently that association is more pronounced at high values of morning BP (more than 20% from mean nocturnal values of SBP).

Adult↗
PubMed1990

Effect of heparin and prostacyclin/heparin infusion on platelet aggregation in hemodialyzed patients.

The number of circulating platelet aggregates determined according to the method of Wu and Hoak and the platelet morphology revealed by scanning electron microscopy were investigated in 10 patients (8 males, 2 females) age 28-58 years) with end-stage renal failure treated by repeated hemodialysis. The examination was carried out twice: during a 4-hour hemodialysis session with the use of heparin alone and 1 week later during the course of another dialysis in the presence of both heparin and prostacyclin. During each dialysis session the platelet system was examined three times: prior to, after 90 min, and at the end of the procedure. As compared with the situation prior to dialysis, the number of platelet aggregates assessed after 90 min of dialysis and after its termination insignificantly rose following the treatment with heparin, but significantly fell after the use of the prostacyclin/heparin combination. The differences were also significant when the effects of both treatment types were compared. As revealed by scanning electron microscopy, during the course of hemodialysis with the use of heparin alone, the platelets showed signs of activation manifested by increases in number and length of cytoplasmic processes and by a tendency to aggregate. When both prostacyclin and heparin were used during dialysis, platelet activation was minimal or absent. Thus, the combined treatment with prostacyclin and heparin protects platelets from activation induced by their contact with artificial surfaces and may lower the risk of microthrombosis, making thereby hemodialysis safer and more effective.

Adult↗
PubMed1990

Differential effect of retinoic acid on ADP and collagen induced platelet aggregation.

Retinoic acid (RA) was found to inhibit ADP induced but not collagen induced aggregation of human platelets and the differential action is related to intraplatelet Ca2+ reflux. RA was active at concentrations as low as 10(-7) M and required 20 min prior incubation with platelet suspension in order to inhibit aggregation by ADP. All the steps in ADP induced but not collagen induced platelet activation, viz. hydrolysis of phosphatidyl inositol, phosphorylation of 20, 47 and 250 kDa proteins as well as increased association of actin with Triton X-100 insoluble cytoskeletal matrix were inhibited by RA. RA when used as an agent for differentiation induction of cell progenitor is likely to affect the platelet aggregation and thereby the haemostatic process.

Adenosine Diphosphate↗
PubMed1991

LY53857, a 5HT2 receptor antagonist, delays occlusion and inhibits platelet aggregation in a rabbit model of carotid artery occlusion.

The present study was designed to evaluate the effectiveness of the ergoline 5HT2 receptor antagonist, LY53857 in a rabbit model of vascular arterial occlusion. LY53857 (1 and 10 microM) inhibited serotonin amplified platelet aggregation responses to threshold concentrations of ADP in rabbit platelets in vitro. LY53857 (1 microM) not only inhibited the serotonin component of rabbit platelet aggregation, but also inhibited in vitro aggregation induced by ADP (48.7 +/- 16.7% inhibition), collagen (76.1 +/- 15.9% inhibition) and U46619 (65.2 +/- 12.3% inhibition). The effectiveness of this ergoline 5HT2 receptor antagonist in blocking aggregation to ADP, collagen and U46619 may be related to its ability to inhibit a serotonin component of platelet aggregation since rabbit platelets possess high concentrations of serotonin that may be released during aggregation produced by other agents. Based on the effectiveness of LY53857 to inhibit rabbit platelet aggregation, we explored the ability of LY53857 to extend the time to carotid artery occlusion in rabbits following electrical stimulation of the artery. Reproducible carotid artery occlusion was induced in rabbits by moderate stenosis coupled to arterial cross clamping, followed by electrical stimulation. With this procedure, occlusion occurred at 47.0 +/- 7 min (n = 30) after initiation of the electrical stimulation. Animals pretreated with LY53857 (50 to 500 micrograms/kg i.v.) showed a delay in the time to carotid artery occlusion (at 100 micrograms/kg i.v. occlusion time extended to 164 +/- 16 min). Furthermore, ex vivo platelet aggregation from animals treated with LY53857 (300 micrograms/kg i.v.) resulted in 40.5% inhibition of platelet aggregation in response to the combination of ADP (1 microM) and serotonin (1 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Inhibition of cyclooxygenase-independent platelet aggregation by sodium salicylate.

The effect of acetylsalicylic acid (ASA) on platelet aggregation (PA) and thromboxane A2 (TxA2) formation was investigated in vitro and ex vivo after 1 g or 300 mg ASA administration to healthy subjects. 50-100 microM ASA inhibited PA by single aggregating agent such as platelet aggregating factor (PAF) or epinephrine and reduced to less than or equal to 5% of control platelet TxB2 formation, but did not influence PA by epinephrine plus PAF. The latter was inhibited by increasing ASA concentration. In samples incubated with 100 microM ASA and stimulated with epinephrine plus PAF, PA could be inhibited by the addition of 100-300 microM sodium salicylate. After 300 mg-1 g ASA administration to healthy subjects, the inhibition of PA by epinephrine plus PAF was more marked by highest doses of ASA. This study suggests that aspirin inhibits PA with a cyclooxygenase-independent mechanism; this effect is mediated, at least in vitro, by salicylic acid.

Adult↗