Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Platelet Aggregation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1981

[Study of platelet aggregation by the filtration pressure method (author's transl)].

Using Hornstra's "filter loop" technique, effects of prostaglandins and vasodilators on ADP-induced platelet aggregation were studied in anaesthetized dogs. ADP-induced platelet aggregation was observed as a transient, reversible elevation of pressure before filter. This pressure change was reproducible and dose-related. PGI2 and PGE1 suppressed the elevation of pressure induced by ADP and decreased the spontaneous elevation of pressure. Thus, it was reconfirmed that PGI2 and PGE1 not only suppressed ADP-induced platelet aggregation but also produced a disaggregation of aggregated platelets. AFter indomethacin, ADP-induced platelet aggregation was potentiated and sometimes became exceedingly protracted, indicating that anti-aggregatory prostaglandin was always present in the circulating blood. Close-injection of bradykinin did not suppress ADP-induced platelet aggregation, while intravenous injection did produce a suppression. After indomethacin, this inhibitory effect was greatly attenuated, indicating a release of anti-aggregatory prostaglandin (PGI2?) by bradykinin. Coronary vasodilators, such as dipyridamole and nifedipine did not inhibit ADP-induced platelet aggregation, nor did sulfinpyrazone. It is concluded that the "filter loop" technique is a useful method that allows aggregation and disaggregation reactions to be followed continuously and quantitatively in the blowing blood. The effects of drugs on platelet aggregation can be assessed in connection with hemodynamic changes such as blood pressure and heart rate induced by systemic administration of the drugs.

Adenosine Diphosphate↗
PubMed1993

Comparative effect of synthetic aminoestrogens with estradiol on platelet aggregation.

The in vitro effect upon platelet aggregation of estradiol and synthetic estrogens (prolame, buame, and proacame) is described. Prolame and buame produced a dose-dependent inhibition on platelet aggregation. Estradiol and proacame did not show anti-aggregating effects. The results suggest that the use of prolame and buame in estrogen therapy could reduce the risk of thrombo-embolic accidents.

Adult↗
PubMed1999

Inhibitory effect of Ginkgo biloba extract on human platelet aggregation.

The effect of pure flavonoids and Gingko biloba extract (GBE) on human platelet aggregation was investigated. Most of the flavonoids and vitamin E did not affect platelet aggregation in platelet-rich plasma (PRP); however some of these flavonoids inhibited platelet aggregation in gel-filtered platelets (GFP). GBE inhibited both ADP- and collagen-induced platelet aggregation in PRP, GFP and in whole blood in a dose-dependent manner. GBE at very low concentrations inhibited whole blood aggregation induced by ADP compared with those used for PRP or GFP. Flavonoids and GBE decreased the production of TxA(2) induced by collagen and ADP in PRP. However, no correlation was observed between the inhibition of platelet aggregation and the decrease of TxA(2) synthesis. GBE and flavonoids did not affect platelet membrane fluidity. However, the incubation of PRP with GBE increased cAMP levels in platelets, which is known to inhibit platelet activation by lowering intracellular Ca2+ levels. GBE is a mixture of many compounds, including flavonoids and gingkoglides, which affect metabolism of cAMP, TxA(2) and Ca2+ in platelets. It is effective in the inhibition of platelet aggregation, both in PRP and whole blood, and thus may be potentially used as an effective oral anti-platelet therapeutic agent.

Journal Article↗
PubMed1986

Platelet aggregation in non-insulin-dependent diabetes is associated with platelet fatty acids.

Platelet aggregation was measured in 15 patients having non-insulin-dependent diabetes mellitus (NIDDM) at the time of diagnosis and after three months of dietary treatment. Mean fasting plasma glucose fell from 13.0 to 8.8 mmol/l (p less than 0.0002), glycosylated haemoglobin fell from a mean of 11.3% to 9.0% (p less than 0.005) and insulin levels fell from a mean of 17.5 to 13.8 mU/l (p less than 0.005). Platelet aggregation showed a variable response and did not correlate with plasma glucose, glycosylated haemoglobin or plasma insulin. Multiple linear regression analysis was carried out on the aggregation values against the biochemical variables and platelet phospholipid fatty acid levels following logarithm transformation. Platelet linolenic acid and eicosapentaenoic acid levels were significantly inversely associated with aggregation but the difference between the relationship at diagnosis and after three months was not statistically significant. The association between platelet omega 3 fatty acids and platelet aggregation suggest that dietary change aimed at increasing the proportions of these fatty acids might favourably influence vascular disease in NIDDM via an effect on platelet function.

Adult↗
PubMed1991

Platelet aggregation in allergic reactions.

The platelet aggregation in the presence of 4 aggregation inducers was studied in 63 allergic patients, consisting of atopic and non-atopic asthmatics and aspirin-sensitive subjects, before and after inhalation tests or in vitro incubation with allergen. Basal platelet aggregation was decreased in 43% of the atopic patients for adrenaline and also in a smaller percentage for other agonists. A decreased aggregation was also observed in 3 out of 6 nonatopic patients and in aspirin-sensitive patients. In vivo or in vitro provocation tests decreased aggregation in some additional patients. These results point out to a compromise of platelets in allergic mechanisms.

Humans↗
PubMed1993

Purification and characterisation of a snake venom phospholipase A2: a potent inhibitor of platelet aggregation.

An inhibitor of human platelet aggregation was identified from the venom of an Australian Copperhead snake, Austrelaps superba, as a novel phospholipase A2. The inhibitor was purified to homogeneity by chromatography on Q-Sepharose, S-Sepharose and C8 reverse phase HPLC. The purified phospholipase A2 has a molecular weight of 15 kDa as assessed by sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). N-terminal sequence analysis of the platelet inhibitor revealed 70-80% sequence identity to other previously described secretory phospholipase A2. Phospholipase activity of the purified protein was confirmed by the ability of the enzyme to hydrolyse lecithin. Pretreatment of the purified protein with the specific phospholipase A2 inhibitor p-bromophenacyl bromide, resulted in abrogation of both its enzyme and platelet inhibitory activity. The phospholipase A2 inhibited platelet aggregation and serotonin release, induced by a variety of platelet agonists, in a time and dose dependent manner.

Amino Acid Sequence↗
PubMed1989

Multifactorial genesis of enhanced platelet aggregability in patients with nephrotic syndrome.

Platelet aggregation, beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) release and thromboxane B2 (TxB2) formation in stimulated platelet-rich plasma were investigated in 13 patients with nephrotic syndrome who had normal serum creatinine levels (creatinine clearance greater than 70 ml/min/1.73 m2). In contrast to 13 sex- and age-matched controls, spontaneous platelet aggregation only occurred in patients with nephrotic syndrome with correlation to serum albumin and plasma fibrinogen levels. The EC50 (estimated concentration of aggregating agent to cause half maximum velocity of primary aggregation) for ADP and collagen and threshold concentration of arachidonic acid (threshold AA) were decreased in patients with nephrotic syndrome, reflecting a hyperaggregable state. In patients with nephrotic syndrome EC50 ADP values were significantly correlated to serum albumin, serum cholesterol and plasma fibrinogen, however, EC50 collagen or threshold AA did not correlate to these parameters. Plasma beta-TG levels were increased in patients, whereas plasma PF 4 levels were not significantly changed in patients compared to controls. In vitro TxB2 formation was elevated in patients only after stimulation with AA. Nevertheless, after stimulation with collagen and ADP, TxB2 formation was unchanged in patients compared to controls. Platelet hyperaggregability in nephrotic patients was confirmed in our study. However, unchanged thromboxane B2 formation after collagen stimulus as well as missing correlations between EC50 collagen or threshold AA and serum albumin were contradictory to the hypothesis that enhanced AA availability due to hypoalbuminemia is responsible for platelet hyperaggregability. Platelet hyperaggregability in terms of EC50 ADP being associated with serum albumin levels as well as to serum cholesterol and plasma fibrinogen indicate a multifactorial genesis.

Female↗
PubMed1984

[Platelet aggregation and resistance to osmotic shock of platelet concentrates obtained by discontinuous-flow cell separation with the surge pump technic].

We studied the ultrastructural morphology and function of platelets collected by apheresis procedure with discontinuous flow using the Surge Pump Technique. The platelet concentrates obtained by this technique are free of erythrocyte and lymphocyte contamination. The platelet morphology as well as the platelet aggregation induced by ADP, adrenaline and collagen of platelet concentrates were similar to those observed in PRP before the apheresis. The response to the hypotonic shock of platelet concentrates was also normal, indicating membrane integrity and good platelet metabolism. These results show that platelet concentrates obtained by the Surge Pump Technique maintain their haemostatic effects and may be infused in thrombocitopenic patients, reducing the risk of alloimmunization related to the presence of erythrocytes and lymphocytes.

Adenosine Diphosphate↗
PubMed1970

Some effects of mucopolysaccharide stains on platelet aggregation.

FIVE MUCOPOLYSACCHARIDE STAINS INHIBIT PLATELET AGGREGATION INDUCED BY SEVERAL AGGREGATING AGENTS: with two stains inhibition is competitive. Alcian blue, 0.05 mg/ml, added to platelet-rich plasma potentiates ADP-induced aggregation. Alcian blue, 0.5 mg/ml, itself produces platelet aggregation, probably causing the release reaction. Three of these stains produce aggregation of red cells. They also bind heparin, and so may influence heparin-neutralizing sites (platelet factor 4) and probably the charge on the platelet membrane. The only known common factor to these stains is their ability to bind onto the mucopoly-saccharides. It is suggested that when platelets are ;stained' the surface mucopolysaccharide is altered and that this alteration can influence platelet aggregation.

Binding Sites↗
PubMed1992

Standardization of platelet aggregation test in normal Thai adults.

Platelet aggregation test was assessed by the turbidimetric method in 52 normal Thai adults consisting of 24 males and 28 females with ages ranging from 20 to 50 years. The aggregating agents used were adenosine diphosphate (ADP), adrenaline and collagen. It was found that the ranges of threshold concentration of ADP, adrenaline and collagen which gave maximal induction of platelet aggregation were 5-10 microM, 2.5-10 microM and 0.14-0.28 mg/mL, respectively. Collagen at the above concentration, showed lag phase within 2 minutes. This corresponds to that described in the reference method. Moreover, when induced by ADP and adrenaline 53-65 per cent and 81-87 per cent of the subjects, respectively, showed biphasic curve. The above concentration of ADP, adrenaline and collagen are suitable for the study of platelet aggregation in normal Thai adults.

Adenosine Diphosphate↗
PubMed2001

Standardized ultrasound as a new method to induce platelet aggregation: evaluation, influence of lipoproteins and of glycoprotein IIb/IIIa antagonist tirofiban.

Most of the published studies concerning platelet aggregation were performed with chemical stimulation procedures, however, mechanical stimulation might be a better simulation of physiological activation of platelets. In order to evaluate the influence of ultrasound on platelet aggregation in vitro, we developed an ultrasound device in a standardized set-up, and we evaluated the influence of lipoproteins and the glycoprotein IIb/IIIa inhibitor tirofiban on ultrasound induced platelet aggregation. A cylindrical shaped plastic test tube with 1 ml of platelet-rich plasma was placed in an ultrasound bath (35 kHz) for 5 s. The ultrasound energy transfer into the sample (Delta W=3.77 J) was calculated using the average temperature increase (averaged by 0.935 degrees C) of the sample. Platelet aggregation was quantified immediately after stimulation with ultrasound or adenosine diphosphate (ADP 2.1 and 4.2 microM) by the Myrenne Aggregometer PA2 at low (40 s(-1)) and afterwards at high (2500 s(-1)) shear. To evaluate the influence of lipoproteins, seven healthy male volunteers were investigated before and after a fat load (50 g fat per m(2) body surface), and 11 patients suffering from hypercholesterolemia and atherosclerotic disease before and after a single low-density lipoprotein (LDL) apheresis. Platelet aggregation after ultrasound stimulation was well correlated with platelet aggregation after ADP (r between 0.50 and 0.95). However, when exposed to high shear, the low shear-induced platelet aggregates were more stable after ultrasound stimulation compared with ADP stimulation either with or without tirofiban. After the fat load triglyceride concentration increased from 0.86+/-0.39 to 2.10+/-1.10 mmol l(-1) (P<0.05) resulting in a reduced formation of platelet aggregates after weak (ADP 2.1 microM) but not after strong (ADP 4.2 microM or ultrasound) stimuli. After a single LDL apheresis LDL cholesterol dropped from 3.99+/-0.90 to 1.06+/-0.55 mmol l(-1) (P<0.005). No changes in platelet aggregation were observed with the exception of a lower aggregation when exposed to high shear after stimulation with 2.1 microM ADP. In conclusion, we found the ultrasound stimulation of platelet-rich plasma easy to perform. The platelet aggregation after ultrasound stimulation correlated well with stimulation after ADP. While a reduction in LDL cholesterol concentration had only slight effects on platelet aggregation, an increase in triglyceride concentration resulted in a reduced formation of platelet aggregates after weak stimulation.

Blood Platelets↗
PubMed1999

Effect of raw versus boiled aqueous extract of garlic and onion on platelet aggregation.

The effects of aqueous extracts of raw and boiled garlic and onions were studied in vitro on the collagen-induced platelet aggregation using rabbit and human platelet-rich plasma. A dose dependant inhibition of rabbit platelet aggregation was observed with garlic. Onion also showed dose-dependent inhibitory effects on the collagen-induced platelet aggregation but this inhibition was of a lesser magnitude compared to garlic when related to dose. The concentration required for 50% inhibition of the platelet aggregation for garlic was calculated to be approximately 6.6 mg ml(-1) plasma, whereas the concentration for onion was 90 mg ml(-1) plasma. Boiled garlic and onion extracts showed a reduced inhibitory effect on platelet aggregation. Garlic but not onion significantly inhibits human platelet aggregation in a dose-dependent fashion. The potency of garlic in inhibiting the collagen-induced platelet aggregation is approximately similar to that of rabbit platelets (8.8 mg ml(-1) produced 50% inhibition of platelet aggregation). The results of this study show that garlic is about 13 times more potent than onion in inhibiting platelet aggregation and suggest that garlic and onion could be more potent inhibitors of blood platelet aggregation if consumed in raw than in cooked or boiled form.

Animals↗
PubMed1982

[Platelet aggregation in hyperlipoproteinemias].

The Authors studied platelet aggregation in 42 hyperlipoproteinemic patients (10 with type IIA familiar, 7 with type IIA, 7 with type IIB, 18 with type IV and V). None of them suffered from clinically detectable vascular complications. The control group included 42 normolipoproteinemic subjects, closely matched for age and sex. Platelet aggregation, according Born's method, was statistically increased in hyperlipoproteinemia type IIA, but only when induced by epinephrine as aggregating agent. No statistical significance was demonstrated when hyperlipoproteinemic smokers and no smokers were compared. A positive family history of myocardial infarction and/or diabetes mellitus could be demonstrate affect on platelet aggregation.

Adolescent↗
PubMed2001

Inhibition of platelet aggregation and the release of P-selectin from platelets by cilostazol.

To evaluate the in vitro effects of cilostazol, a phosphodiesterase III inhibitor, on platelet responses, we measured platelet aggregation and the levels of soluble P-selectin, a glycoprotein present on the alpha-granule membrane in resting platelets, and cAMP. Platelet-rich plasma and washed platelets from healthy human volunteers were treated with cilostazol (5, 25 and 50 microM). Platelet-rich plasma was stimulated by ADP (1 and 5 microM) or collagen (5 microg/ml). Washed platelets were stimulated by thrombin (4 U/ml) in the presence or absence of 1 microM forskolin. In vehicle-treated samples, soluble P-selectin levels in response to 1 microM ADP-induced primary aggregation were similar to those of circulating levels of healthy volunteers but the levels in response to 5 microM ADP-induced secondary aggregation and collagen-induced aggregation increased markedly compared to those in response to primary aggregation. This result suggests that P-selectin is released from platelets according to the extent of platelet aggregation. Cilostazol inhibited platelet aggregation as well as P-selectin release in a concentration-dependent manner. Cilostazol inhibited completely thrombin-induced aggregation in the presence of 1 microM forskolin, when cAMP levels were two-fold higher than those in the absence of forskolin. Cilostazol, which increases intracellular cAMP in platelets, may be useful in the treatment of arterial occlusive diseases.

Adenosine Diphosphate↗
PubMed1998

In vivo and in vitro studies of the inhibitory effect of propofol on human platelet aggregation.

BACKGROUND: The inhibitory effects of propofol on platelet aggregation are controversial because the fat emulsion used as the solvent for propofol may affect platelet function. The effects of propofol on platelet intracellular calcium ion concentration and on aggregation were investigated. METHODS: Platelet aggregation was measured in 10 patients who received an intravenous infusion of propofol. Intralipos, the propofol solvent, was infused in 10 healthy volunteers and platelet aggregation were measured. The in vitro effects of propofol and Intralipos on platelets were also investigated. The inhibitory effects of various concentrations of propofol were studied. The effects of propofol on the changes in intracellular calcium level using a fluorescent dye, fura-2, were also observed. Template bleeding time was measured to determine the effect of propofol in clinical use. RESULTS: Platelet aggregation was significantly inhibited by infusion of propofol, although bleeding time was not prolonged. Intralipos did not inhibit platelets either in vivo or in vitro. Propofol significantly inhibited platelet aggregation in vitro and at 5.81 +/- 2.73 microg/ml but not at 2.08 +/- 1.14 microg/ml. The increase of intracellular calcium concentration was inhibited both in influx and discharge of calcium. CONCLUSIONS: Propofol inhibited platelet aggregation both in vivo and in vitro. Inhibition of platelet aggregation appeared to be caused by propofol itself and not by the fat emulsion. This inhibitory effect was also supported by the suppressed influx and discharge of calcium. No change in the bleeding time suggests that this inhibitory effect does not impair hemostasis clinically.

Adult↗
PubMed1982

Inhibition of platelet aggregation by ethanol in vitro shows specificity for aggregating agent used and is influenced by platelet lipid composition.

Ethanol at physiologically tolerable concentrations inhibited platelet aggregation in vitro in a relatively specific way, which may be influenced by platelet membrane lipid composition. Aggregation to collagen, calcium ionophore A23187 and thrombin (low doses) were often markedly inhibited by ethanol, adrenaline and ADP responses were little affected, and aggregation to exogenous arachidonic acid was actually potentiated by ethanol. Aggregation to collagen, thrombin and A23187 was inhibited more by ethanol in platelets enriched with saturated fatty acids than in those enriched with unsaturated fats. Platelets enriched with cholesterol showed increased sensitivity to ADP, arachidonate and adrenaline but this increase in cholesterol content did not appear to influence the inhibition by ethanol of platelet responses. The results suggest that ethanol may inhibit aggregation by an effect on membrane fluidity and/or calcium mobilization resulting in decreased activity of a membrane-bound phospholipase.

Adenosine Diphosphate↗
PubMed2006

Propyl gallate-induced platelet aggregation in patients with end-stage renal disease: the influence of the haemodialysis procedure.

BACKGROUND: Platelet dysfunction is a well-established disturbance in haemodialysis (HD) patients. Propyl gallate is a synthetic platelet activator with the property to stimulate platelet aggregation. The aim of the present study was to evaluate the influence of a single haemodialysis session on propyl gallate-induced platelet aggregation. METHODS: Thirty-nine HD patients were enrolled in the study and 20 healthy volunteers were studied as controls. Cellulose diacetate (CD) dialysers were used in 20 patients and polysulphone dialysers in 19. HD was performed via an A-V fistula in 27 patients and via an i.v. catheter in 12. Erythropoietin was administered in 37 patients (epoietin-alpha in 24 and darbepoietin in 13). Thirty-four were receiving the low-molecular-weight heparin tinzaparin. Propyl gallate slide aggregometry was used for evaluating platelet aggregation. RESULTS: In HD patients, platelet aggregation was impaired before as well as after the HD session. No effect of the HD procedure, type of vascular access, adequacy of HD or type of erythropoietin on the propyl gallate-induced platelet aggregation was detected. Platelet aggregation was higher when CD dialyser was used. A negative correlation between the time needed for platelet aggregation to occur and tinzaparin dose was found. CONCLUSION: Propyl gallate-induced platelet aggregation in HD patients is impaired. Platelet aggregation was higher in patients dialysed with CD membrane than in those dialysed with polysulphone membrane. The higher the dose of tinzaparin, the higher the platelet aggregation. The clinical significance of the above results needs further evaluation.

Female↗
PubMed1987

Platelet-activating factor: mediator of the third pathway of platelet aggregation? A study in three patients with deficient platelet-activating factor synthesis.

Thrombin, collagen, and Ca2+-ionophore A23187 aggregate platelets in the presence of inhibitors of the first (ADP-mediated) and second (cyclooxygenase-dependent) pathway of platelet activation. This aggregation, via a third pathway, was hypothesized to be mediated by the alkoxyether lipid platelet-activating factor (PAF). We recently demonstrated virtual absence of plasmalogen-type alkoxyether lipids and deficiency in key enzymes of their biosynthesis in Zellweger patients. We hypothesized that PAF synthesis might also be impaired. We report two Zellweger patients with an undetectable A23187-induced PAF synthesis of leukocytes (patients, less than 3 pmol PAF/10(8) granulocytes (PMN); four age-matched controls, 249-2,757 pmol PAF/10(8) PMN; five adult controls, 291-5,433 pmol PAF/10(8) PMN). In a third patient, residual PAF synthesis was detected. However in all patients the thrombin-induced third mechanism of platelet aggregation was present. We therefore conclude that PAF may not be the mediator of the third pathway.

Abnormalities, Multiple↗