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At least 1,369 records · Page 76Linked to original sources
PubMed1994

Calpain-induced down-regulation of protein kinase C inhibits dense-granule secretion in human platelets. Inhibition of platelet aggregation or calpain activity preserves protein kinase C and restores full secretion.

The relationship between platelet aggregation, calpain activation, PKC activities and the secretory response have been examined in PMA-and ionomycin-stimulated platelets. Co-addition of PMA and ionomycin resulted in a maximal synergistic secretion of [14C]5-hydroxytryptamine ([14C]5-HT) from platelet dense granules. However, prior addition of PMA for 5 or 10 min resulted in a reduction of this secretory response. Inclusion of either RGDS (to inhibit platelet aggregation) or E64-d (to inhibit calpain activity) resulted in full restoration of the secretory response. In experiments to determine the activity status of PKC, PMA was found to induce a loss in cytosolic and total PKC activity without an increase in membrane-associated activities during this time period. Inhibition of either platelet aggregation or calpain activity resulted in preservation of total and cytosolic activities with a measurable increase in membrane translocated activity. PMA-induced phosphorylation of a number of PKC substrates was measured in 32P-labelled platelets. PMA induced potent phosphorylation of the 45 and 20 kDa species and also proteins of the molecular masses 66, 80, 97 and 119 kDa. Phosphorylation was maximal at either 1 or 2 min after which dephosphorylation occurred. Inclusion of either RGDS or E64-d resulted in a reduction of the dephosphorylation rates, and sustained phosphorylation of the 66, 80, 97 and 119 kDa proteins. These studies suggest that the activity status of PKC is an important factor in the level of secretion obtained and that platelet aggregation is involved in calpain-initiated down-regulation of PKC.

Blood Platelets↗
PubMed2002

Effect of increasing doses of aspirin on platelet aggregation among stroke patients.

BACKGROUND AND PURPOSE: Aspirin has been shown to reduce the risk of myocardial infarction and stroke. Some investigators believe that low-dose aspirin inhibits platelet aggregation to the same degree as high-dose aspirin. Our study aimed to assess the effect of increasing doses of aspirin on the degree of platelet aggregation induced by collagen and adenosine diphosphate (ADP) among stroke patients. METHODS: Sixteen poststroke patients were prescribed aspirin at daily doses of 40, 80, 160, 325, 650, and 1,300 mg, each dose to be taken for 14 days (total duration 12 weeks). Platelet aggregation studies using 2 microgram/ml collagen and 2 microM ADP were performed on platelet-rich plasma at baseline and on the 14th day of each dose. RESULTS: Platelet aggregation studies using 2 microgram/ml collagen at the start of treatment and at the 14th day of each dose revealed dose-dependent inhibition by aspirin starting at 40 mg/day, but was optimal at 80- 160 mg/day. ADP-induced platelet aggregation inhibition appears to be dose dependent up to 1,300 mg/day. CONCLUSION: Inhibition of collagen-induced platelet aggregation by aspirin appears to be optimal at 80-160 mg/day, while ADP-induced platelet aggregation inhibition by aspirin appears to be dose dependent up to 1,300 mg/day in our poststroke patients, albeit to a less remarkable degree at higher doses.

Adenosine Diphosphate↗
PubMed1982

[In vitro effect of culture fluids from neoplastic tissues on platelet aggregation. I. Human tumors of the gastrointestinal tract].

The effects on platelet function of culture media from 7 human tumours of the gastroenteric tract have been studied on platelet rich plasma obtained from 28 apparently normal subjects. Platelet aggregation was investigated according to Born's method. Some of the culture media showed an aggregating activity on platelets, while others did not; after dialysis, however, also the last ones aggregated platelets. Furthermore all the media both before and after dialysis were able to increase the platelet response to low doses of ADP (3 microM), and these effects were inhibited by Aspirin (0,1 mM). These results suggest that the tumours investigated release stimulating activities on platelet function and that these interactions can be inhibited pharmacologically.

Adenosine Diphosphate↗
PubMed1996

Proteolysis of thrombospondin during cathepsin-G-induced platelet aggregation: functional role of the 165-kDa carboxy-terminal fragment.

The serine-proteinase cathepsin G (CG) is a potent agonist of platelet aggregation inducing the release and surface expression of alpha-granule adhesive proteins such as fibrinogen (Fg) and thrombospondin-1 (TSP-1). Because Fg and TSP-1 are potential substrates for the enzymatic activity of CG, we investigated the fate of these proteins during CG-induced platelet aggregation using an immunoblot technique. Only a small proportion of secreted Fg was proteolyzed by CG and platelet aggregation was efficiently inhibited by anti-fibrinogen Fab fragments. In contrast, TSP-1 was extensively proteolyzed on aggregated platelets releasing in the milieu a fragment with Mr approximately 28 000, corresponding to the amino-terminal heparin-binding domain (HBD). Several antibodies, directed against the cell-associated carboxy-terminal TSP-1f fragment (Mr approximately 165000) impaired the formation of stable macroaggregates, indicating that this fragment may contribute to platelet aggregation in the absence of the HBD.

Adult↗
PubMed1975

Plasma components which interfere with ristocetin-induced platelet aggregation.

Normal human plasma contains a component or components which interfere with ristocetin-induced platelet aggregation. Preliminary examination suggests a protein (or proteins) which binds ristocetin and competes more effectively for ristocetin than do the proteins involved in ristocetin-induced platelet aggregation. The presence of this protein in normal human plasma also prevents ristocetin-induced precipitation of plasma proteins at levels of ristocetin necessary to produce platelet aggregation (0.5-2.0 mg/ml). Serum contains an apparent two0fold increase of this component when compared with plasma. Heating serum at 56 degrees for one hour results in ad additional 2 to 4 forl increase. The presence of a ristocetin-binding protein in normal human plasma requires that this protein be saturated with ristocetin before ristocetin-induced platelet aggregation will occur. Variations in the ristocetin-binding protein(s) will cause apparent discrepancies in ristocetin-induced platelet aggregation in normal human plasmas.

Adsorption↗
PubMedDate not supplied

Effect of naftidrofuryl and aspirin on platelet aggregation in peripheral vascular disease.

Platelet aggregation in whole blood (WB) was assessed in healthy subjects and in patients with peripheral vascular disease (PVD) using a WB-free platelet counting (WB-FPC) method. Aggregation induced by stirring and platelet agonists was significantly enhanced in PVD patients. WB-FPC aggregation induced by 5-HT was diminished significantly by incubation with naftidrofuryl (NAF) in WB of PVD patients. In contrast, aspirin (acetylsalicylic acid; ASA), added in vitro, did not significantly affect 5-HT or stirring-induced WB-PFC aggregation in PVD patients. Furthermore, 5-HT-induced WB-FPC was inhibited by NAF in blood collected from PVD patients that were taking low dose aspirin. These findings suggest that NAF may be of benefit to patients with hyperaggregable platelets and elevated plasma 5-HT concentrations, factors thought to predispose to thrombotic complications.

Adult↗
PubMed1989

Arterial thrombosis associated with immune thrombocytopenia: presence of a platelet aggregating IgG synergistic with thrombin and adrenalin.

We report the case of a 50-year-old lady who presented with arterial thrombosis in the setting of thrombocytopenia. Investigations confirmed the diagnosis of idiopathic thrombocytopenic purpura. A spontaneous platelet aggregating factor (SPAF) was isolated from the immunoglobulin fraction of the patient's plasma. The isolated IgG irreversibly aggregated platelet-rich plasma and washed platelets, an effect abolished by pretreating the platelets with aspirin. The activity of the IgG was greatly enhanced by subaggregatory concentrations of thrombin and adrenalin and was localized to the F(ab')2 of the molecule. Plasmapheresis in combination with anti-platelet therapy resulted in an increase in the patient's platelet count, reduced platelet aggregating activity of plasma and significant clinical improvement. We suggest that the presence of this platelet aggregating IgG contributed to the development of thrombosis in our patient and postulate that a similar factor may explain the paradox of thrombosis observed in a select group of thrombocytopenic patients.

Blood Platelets↗
PubMed1976

Substituted alpah-methylbenzyl and tricyclic arylalkyl lactamimides as inhibitors of blood platelet aggregation.

N-[1-(p-Phenoxyphenyl)ethyl]hexahydro-2H-azepin-2-imine hydrochloride (10) and N-[1-(2-dibenzothienyl)-ethyl]hexahydro-2H-azepin-2-imine hydrochloride (22) were found to inhibit in vitro aggregation of human blood platelets induced by ADP with minimal release of procoagulant platelet factor 3. The compounds were selected from a series of substituted alpha-methylbenzyl and tricyclic arylalkyl lactamimides that were free of hypoglycemic and diuretic effects. Compounds 10 and 22, as well as N-[1-(1-naphthyl)ethyl]hexahydro-2H-azepin-2-imine hydrochloride (I) and N-(2,2-diphenylpentyl)hexahydro-2H-azepin-2-imine hydrochloride (II), were evaluated for effects on ADP-induced platelet aggregation after repeated oral administration to guinea pigs. Compound II (RMI 12,366A) showed in vivo activity in this system 2 h after the last of four daily doses of 100 mg/kg po.

Adenosine Diphosphate↗
PubMed2003

Inhaled NO inhibits platelet aggregation and elevates plasma but not intraplatelet cGMP in healthy human volunteers.

Effects of inhaled nitric oxide (NO) on human platelet function are controversial. It is uncertain whether intraplatelet cGMP mediates the effect of inhaled NO on platelet function. We investigated the effect of 30 ppm inhaled NO on platelet aggregation and plasma and intraplatelet cGMP in 12 subjects. We performed platelet aggregation studies by using a photooptical aggregometer and five agonists (ADP, collagen, epinephrine, arachidonic acid, and ristocetin). During inhalation, the maximal extent of platelet aggregation decreased by 75% with epinephrine (P < 0.005), 56% with collagen (P < 0.005), and 20% with arachidonic acid (P < 0.05). Responses to ADP (8% P > 0.05) and ristocetin (5% P > 0.05) were unaffected. Platelet aggregation velocity decreased by 64% with collagen (P < 0.005), 60% with epinephrine (P < 0.05), 33% with arachidonic acid (P < 0.05), and 14% with ADP (P > 0.05). Plasma cGMP levels increased from 2.58 +/- 0.43 to 9.99 +/- 5.57 pmol/ml (P < 0.005), intraplatelet cGMP levels were unchanged (means +/- SD: 1.96 +/- 0.58 vs. 2.71 +/- 1.67 pmol/109 platelets; P > 0.05). Inhaled NO inhibits platelet aggregation via a cGMP independent mechanism.

Administration, Inhalation↗
PubMed1991

[The effect of finoptin on platelet aggregation, blood coagulability and fibrinolysis in patients with ischemic heart disease during physical exercise].

Exercise platelet aggregation, blood coagulability, and fibrinolysis were examined in patients prior myocardial infarction 2-3 months following the disease. Seventy patients of whom 35 had received placebo and 35 finoptin prior to exercise were studied. The platelet aggregation, blood coagulability, and fibrinolysis were explored before and after bicycle ergometric test. Following exercise, the patients on placebo showed higher platelet aggregation, blood coagulability and lower fibrinolysis, whereas those on finoption exhibited a lower increase in platelet aggregation and blood coagulability and activated fibrinolysis.

Adult↗
PubMed1990

Prevention of canine coronary artery thrombosis with echistatin, a potent inhibitor of platelet aggregation from the venom of the viper, Echis carinatus.

A model of acute, platelet-dependent canine coronary artery thrombosis was utilized to assess the antithrombotic effect of a synthetic, RGD-containing 49-residue protein termed echistatin. This protein is derived from the venom of the viper, Echis carinatus. In vitro, echistatin inhibited ADP (10 microM)-induced platelet aggregation with IC50 values in human and canine platelet-rich plasma of 101 +/- 4 and 127 +/- 32 nM, respectively. In vivo, in the dog, infusion of echistatin for 30 min at 20 micrograms kg-1 min-1 or 2.6 nM kg-1 min-1 resulted in total abolition of acute platelet-dependent coronary thrombus formation in all dogs tested (n = 5). Infusion of a lower dose (10 micrograms kg-1 min-1) was not effective in prevention of thrombus formation. Blood samples were taken before and after infusion of echistatin in order to determine ex vivo platelet aggregatory responses. Echistatin (20 micrograms kg-1 min-1, i.v.) attenuated ex vivo platelet aggregation elicited by ADP, U-46619 and collagen and increased bleeding time by 2.9 +/- 0.5-fold over control. Thus, in the dog, echistatin is an effective antithrombotic agent inhibiting both platelet aggregation in vivo in the coronary artery as well as ex vivo with a concomitant increase in bleeding time. Furthermore, the effects of echistatin on platelet aggregation and bleeding time are reversible with restoration to control levels occurring 30-60 min after termination of the infusion.

Animals↗
PubMed1988

Individual variation in platelet aggregability and serum thromboxane B2 concentrations after low-dose aspirin.

The effects of low daily oral doses of aspirin (40 mg/day) on platelet aggregability and serum thromboxane B2 concentrations were studied in 19 poststroke patients. Although platelet aggregation was reduced significantly after 1 week, there was wide individual variation in the inhibition of platelet function in spite of marked decreases of serum thromboxane B2 concentrations by greater than 90% (from 224 +/- 58 to 8 +/- 8 ng/ml). There was no correlation between collagen-induced platelet aggregability and serum thromboxane B2 concentration before aspirin administration in the range 100-350 ng/ml, but after 1 week of repeated administration of aspirin, there was a correlation between platelet aggregability and serum thromboxane B2 concentrations of less than 25 ng/ml (r = 0.68, p less than 0.01). However, platelet inhibition was insufficient even in some patients with markedly decreased thromboxane B2 concentrations (less than 5 ng/ml). Our results suggest that individual variation of platelet aggregability in response to low-dose aspirin may be due to variation not only in the degree of inhibition of thromboxane A2 production but also in the relative dependence of platelet aggregation on extra-arachidonic pathways.

Aged↗
PubMed1997

Effects of aspirin on platelet aggregation in smokers and nonsmokers.

OBJECTIVE: To assess the relative antiaggregatory ability of aspirin on platelets of smoking and nonsmoking healthy volunteers. DESIGN: Prospective, randomized, crossover study. SETTING: Tertiary-care teaching institution. SUBJECTS: Eighteen healthy smoking and nonsmoking male volunteers. INTERVENTIONS: Each subject received aspirin 325 mg or ticlopidine 250 mg bid as an active control for 7 days in a crossover manner separated by a 1-month washout period. Whole blood platelet aggregation was measured on four occasions, twice at baseline and once after each drug treatment. OUTCOME MEASUREMENT: Whole blood ex vivo platelet aggregation in terms of impedance (omega) and adenosine triphosphate (ATP) release (nmol), as assessed using Lumi-aggregometry. RESULTS: Aspirin was associated with significantly less ATP release in both smokers (p = 0.01) and nonsmokers (p = 0.003). No significant differences in platelet aggregation were found between smokers and nonsmokers at baseline or with any treatment phases. Sixty-seven percent and 17% of volunteers receiving ticlopidine and aspirin, respectively, reported adverse effects. CONCLUSIONS: Twice-daily administration of aspirin for 7 days to healthy volunteers was well tolerated and also reduced platelet aggregation significantly regardless of smoking status.

Adenosine Triphosphate↗
PubMed1992

Effect of albumin on the inhibition of platelet aggregation by beta-lactam antibiotics.

Platelet aggregation and bleeding time abnormalities are reported in patients receiving beta-lactam antibiotics (beta LAs), although clinical bleeding most frequently occurs in chronically ill, malnourished patients. Although most beta LAs bind to serum albumin, the relative influence of bound versus unbound beta LAs on platelet function is unknown. We examined the effect of beta LAs on the aggregation of gel-filtered platelets from normal subjects and on platelet-rich plasma (PRP) from hypoalbuminemic patients. Therapeutic concentrations of five beta LAs were added to normal platelets at different albumin concentrations (1.5 to 4.5 g/dL). Inhibition of aggregation by the beta LAs was inversely proportional to the albumin concentration, and most antibiotic-treated samples showed more than 50% inhibition at albumin levels below 2.0 g/dL. When PRPs from hypoalbuminemic patients were incubated with cephalothin, aggregation was completely inhibited, in contrast to samples from patients with normal albumin levels, and this decreased platelet aggregation was partially restored (25% to 75%) by increasing the albumin concentration above 4.0 g/dL. Specific binding of [35S]-benzylpenicillin to normal platelets decreased proportionately as the albumin concentration increased in the range of 1.0 to 5.0 g/dL. The inhibitory effects of beta LAs on platelets in vitro appear to be influenced by albumin concentration. Plasma albumin concentration may influence bleeding in patients receiving beta LAs.

Anti-Bacterial Agents↗
PubMed1989

Platelet aggregability in sleep-related stroke.

We examined platelet aggregability during nocturnal sleep and daytime wakefulness in patients with a history of sleep-related stroke onset (SOS) and compared it to that of matched awake-onset stroke (AOS) patients and controls without evidence of vascular disease. Aggregability was evaluated in-vitro at least seven weeks following stroke onset. Platelets were more aggregable to ADP, collagen and arachidonic acid (AA) during both sleep and wakefulness in patients with AOS (p less than 0.01). No significant difference in the mean aggregation thresholds during sleeping or waking periods were found between SOS and control groups. However, platelets were significantly more responsive to AA during sleep than during wakefulness in the SOS patients (p less than 0.01). This difference was confined to the subgroup of SOS patients who had experienced nocturnal as opposed to daytime sleep-related stroke onset, suggesting that the observed difference in platelet responsiveness to AA may be related to a circadian fluctuation in platelet aggregability rather than to a sleep-related fluctuation. Significant sleep-related changes in platelet aggregability were not identified in the other two groups.

Adenosine Diphosphate↗
PubMed1989

A new hypoglycemic agent, midaglizole, blunts diabetic platelet aggregation: a possible role of alpha 2 blockade.

A newly developed alpha 2 blocker, midaglizole (DG-5128, 2-[2-(4,5-dihydro-1H-imidazol-2-yl)-1-phenylethyl] pyridine dihydrochloride sesquihydrate) has been shown to have a hypoglycemic action in healthy controls as well as in diabetics. Since human platelets are rich in alpha 2 receptors, the effects of midaglizole on platelet aggregation were investigated. In normal controls, ADP- or epinephrine-induced platelet aggregation was significantly inhibited 2 h after oral administration of 300 mg midaglizole. Midaglizole also suppressed diabetic platelet aggregation stimulated by 10 or 100 microM epinephrine and delayed the initiation of collagen-induced aggregation at 30 micrograms/ml. In vitro addition of midaglizole at 9 or 90 microM significantly inhibited epinephrine-induced platelet aggregation. Furthermore, long-term administration of midaglizole suppressed diabetic platelet aggregation induced by 0.5-1 microM ADP or 1 microM epinephrine. These results suggest that alpha 2 blockade not only blunts diabetic epinephrine-induced platelet aggregation but also affects ADP- or collagen-stimulated platelet aggregation, indicating that this alpha 2 blocker may offer a new approach to the treatment of diabetic microangiopathy.

Adrenergic alpha-Antagonists↗
PubMed1985

Platelet activity in mitral valve prolapse: a study of platelet aggregation, malondialdehyde production, and plasma beta-thromboglobulin.

Platelet aggregation, malondialdehyde (MDA) production, and recovery after aspirin (ASA) administration and plasma levels of beta-thromboglobulin (BTG) were determined in 40 asymptomatic patients with mitral valve prolapse (MVP) and 17 normal subjects. Platelet aggregation was similar in patients and controls, although two patients presented spontaneous aggregation. Production of MDA and plasma levels of BTG were higher in MVP than in controls; however, recovery after ASA was similar in both groups. The results further indicate that platelet hyperactivity is present in a significant number of asymptomatic patients with MVP.

Adolescent↗
PubMed1982

Inhibitory mechanism of dipyridamole on platelet aggregation ex vivo.

The effects of dipyridamole on platelet aggregation ex vivo and in vitro and on platelet cyclic AMP phosphodiesterase (PDE) were studied, and the mechanism of the ex vivo effects was assessed. Both the ADP- and collagen-induced aggregations ex vivo were inhibited dose-responsively by oral administration of dipyridamole. Maximum dipyridamole levels in the plasma were reached at 30 min after the administration. The inhibitory effects of dipyridamole on platelet aggregation ex vivo reached a maximum at between 1 and 2 hrs. On the other hand, the ADP-induced aggregation in vitro and cyclic AMP PDE activity were not inhibited until after 10 min of incubation at a low concentration of dipyridamole. This mode of inhibition of platelet aggregation in vitro and of cyclic AMP PDE activity agreed with the mode of inhibition in the case of platelet aggregation ex vivo. It is suggested therefore that the ex vivo effects, observed with only a low dipyridamole concentration in the plasma, may be due primarily to inhibition by dipyridamole of the cyclic AMP PDE in platelets.

Adenosine Diphosphate↗