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PubMed2001

Possible effects of antioxidant status on increased platelet aggregation in childhood iron-deficiency anemia.

BACKGROUND: Alterations in platelet function and antioxidant status in children with iron-deficiency anemia (IDA) have been reported previously. The present study was performed to better understand possible interactions between these two systems. METHODS: Erythrocyte superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activity and platelet function were evaluated in 15 children (aged 1 1/2-15 years) with IDA. The antioxidant enzyme activity was determined spectrophotometrically. Platelet aggregation and secretion studies were performed using impedance and bioluminescence methods, respectively. Ten age-matched healthy children were included as a control group. RESULTS: There were no differences in SOD and CAT activities between patients and controls. However, GSH-Px activity was significantly lower in the iron-deficient children. Platelet aggregation responses to collagen and ADP were also significantly higher in iron-deficient children than in controls. CONCLUSIONS: Decreased antioxidant defense in IDA may cause increased oxidant stress, which, in turn, may result in a tendency towards platelet aggregation.

Adolescent↗
PubMed1978

Platelet aggregation in aortic and coronary venous blood in patients with and without coronary disease. 3. Role of tachycardia stress and propranolol.

We studied 16 patients with coronary artery disease (CAD) to evaluate platelet aggregation in blood samples withdrawn simultaneously from the aorta and coronary sinus. At rest, mean platelet aggregation in coronary venous blood was significantly lower than that in aortic blood. Platelet counts in coronary venous blood were also lower than in the aortic blood in each of the six CAD patients in whom counts were done. Platelet aggregation was lower in seven patients who were taking propranolol than in the remaining nine who were not taking propranolol. During tachycardia stress, platelet aggregation increased in all patients, but the magnitude of increase was greater in patients not taking propranolol. In four other patients without CAD, platelet aggregation and counts were also studied in the same fashion and were similar in both the aortic and coronary venous blood. These data suggest that in certain CAD patients, platelet consumption or destruction within atherosclerotic vasculature may occur. Propranolol may reduce platelet aggregation at rest and modify excessive aggregation during tachycardia stress in certain CAD patients.

Aorta↗
PubMed1992

New indole and triazino[5,4-b]indol-4-one derivatives: synthesis and studies as inotropics and inhibitors of blood platelet aggregation.

New triazino[5,4-b]indol-4-one derivatives carrying amino groups in position 3 were synthetized and tested as inotropic agents and inhibitors of platelet aggregation. 2h, 2p, 5p, and 6g are the most active as inotropic agents. Compounds were tested as inhibitors of platelet aggregation induced by adenosine 5'-diphosphate (ADP) and arachidonic acid (AA) (guinea pig whole blood). 2k, 2p, 5o, 6d, 6m, and 6o are the most active as inhibitors of the platelet aggregation induced by AA. 6d, 6h, and 6o are most active compounds also in the aggregation induced by ADP. Radioimmunoassay studies, following AA induced aggregation, measuring thromboxane B2 (TXB2) and prostaglandin E2 (PGE2) were carried out on compounds 2b, 2d, 2f, 2g, 2h, 2i, 2k, 2m, 2o, 2p, 2r, 5i, 5j, 5k, 5r, and 5f, which inhibit platelet aggregation induced by AA. None of the compounds tested turned out to be selective inhibitors. Compounds 2h and 2p showed both inotropic and platelet aggregation inhibiting activity.

Animals↗
PubMed1990

Inhibition of human platelet aggregation and thromboxane-B2 production by melatonin: evidence for a diurnal variation.

The effects of melatonin on platelet aggregation and thromboxane-B2 (TxB2) production induced by 1-4 x 10(-6) M adenosine diphosphate (ADP) or 0.6 x 10(-3) M arachidonic acid (AA) were assessed in platelet-rich plasma (PRP). Micromolar concentrations of melatonin inhibited in a dose-dependent way ADP-induced platelet aggregation with individual inhibitions 40% or more at 10(-6)-10(-5) M. A significant depression of AA-induced platelet aggregation was observed only at 10(-5)-10(-4) M melatonin. Morning (0830 h)-evening (1800 h) studies of ADP-induced platelet aggregation in seven normal men showed a higher sensitivity at 1800 h when analyzed as a global inhibitory effect of melatonin (P less than 0.01). Moreover, only during the evening hours did melatonin induce reversible aggregation, an index of inhibition of the platelet secretory process elicited by ADP exposure. No diurnal variability in melatonin inhibition of AA-induced aggregation was detected. TxB2 production elicited by AA in the evening was inhibited significantly in a concentration-related manner by a 2-min preincubation with 10(-9)-10(-5) M melatonin, while during the morning hours the inhibition was significant only at 10(-6) M or higher melatonin concentrations. In the case of ADP, the inhibition of TxB2 release attained significance at 10(-5)-M (0830 h) or 10(-6)-M concentrations (1800 h). In the presence of either stimulatory agent, melatonin depression of TxB2 generation was about 2-fold greater at 1800 h than at 0830 h. The diurnal changes in melatonin effect on TxB2 production were also observed in thrombin-stimulated washed platelets. The present data indicate the existence of circadian variations in platelet responsiveness to melatonin in humans.

Adult↗
PubMed2005

Short-term, moderate dosage Vitamin E supplementation may have no effect on platelet aggregation, coagulation profile, and bleeding time in healthy individuals.

OBJECTIVE: To investigate the in vivo effect of short-term, moderate dosage synthetic dl-alpha-tocopherol acetate supplementation on platelet aggregation, coagulation profile, and simulated bleeding time in healthy individuals. alpha-tocopherol is the most biologically active isomer of Vitamin E, traditionally promoted as an antioxidant and therapeutic agent in cardiovascular disease. In vitro studies have suggested that alpha-tocopherol plays a role in the inhibition of platelet aggregation. However, further investigations into the effect of alpha-tocopherol on bleeding in vivo have not duplicated these findings. MATERIALS AND METHODS: A total of 42 healthy volunteers complied with a 2-week abstinence period from the use of anti-platelet agents followed by determination of baseline platelet aggregation properties and coagulation studies using citrated whole blood. Moderate dosage Vitamin E (800 IU of dl-alpha-tocopherol acetate) was then self-administered for 14 days with reevaluation of platelet aggregation and coagulation profile, and simulated bleeding time after 14 days of Vitamin E supplementation. RESULTS: Forty subjects completed the 4-week study period. All 40 subjects demonstrated normal baseline coagulation studies and all had collagen-stimulated platelet aggregation assessment performed in triplicate. After Vitamin E supplementation, no significant difference was demonstrated in any study parameter. CONCLUSIONS: Dietary supplementation with moderate dosage synthetic dl-alpha-tocopherol acetate did not significantly prolong bleeding or platelet aggregation in vivo. The affect of Vitamin E on platelet aggregation in vitro does not appear to be reproducible in vivo. Therefore, peri-operative discontinuation of Vitamin E may not be necessary.

Adenosine Diphosphate↗
PubMedDate not supplied

Effects of garlic extract on platelet aggregation: a randomized placebo-controlled double-blind study.

1. Studies of the effects of garlic on platelet aggregation have produced inconsistent results possibly related to variations in study design and in the garlic preparations used. 2. The present study examined the effects on platelet aggregation and serum thromboxane and lyso-platelet activating factor, of feeding garlic extract to healthy men using a placebo-controlled, double-blind design. The effects of the same garlic preparation on platelet aggregation in vitro were also investigated. 3. There were no significant differences in platelet aggregation with adenosine diphosphate, platelet activating factor (PAF) or collagen according to treatment group. Serum thromboxane and lysoPAF also showed no change related to garlic supplements. 4. In vitro aggregation with collagen decreased linearly with increasing amounts of garlic extract, but concentrations were higher than those attainable in vivo. Gastrointestinal side effects prevented the use of higher doses of garlic which must be considered to be pharmacological as they exceed changes achievable by dietary modification.

Adenosine Diphosphate↗
PubMed1981

[Dependence of blood platelet aggregation capacity on agents affecting the intrathrombocyte Ca2+ content].

The effect of agents changing absorption and redistribution of Ca2+ in platelets on platelet aggregation was studied. It was shown that inhibition of intercellular Ca2+ absorption by verapamil and tetracain block of intracellular Ca2+ redistribution decrease platelet aggregation. A joint action of verapamil and tetracain increase the inhibition of aggregation. EDTA decreases platelet aggregation affecting platelet regulatory mechanisms associated with the action of cAMP and probably directed at a decrease in the platelet cytoplasmic Ca2+ content.

Adenosine Diphosphate↗
PubMed2000

Effect of naftidrofuryl on platelet aggregation in plasma from aspirin treated patients: an in vitro study.

This study concerns an in vitro evaluation of the effect of naftidrofuryl on platelet aggregation in plasma of 15 diabetic patients, who were being treated with aspirin, and who were suffering from chronic arterial disease of the lower limbs. Platelet aggregation, induced either spontaneously or by aggregating agents, was measured in platelet-rich plasma (PRP). The results show that serotonin (5-HT)- and adenosine 5'-diphosphate (ADP)-induced platelet aggregation significantly decreased after addition of naftidrofuryl. Decreases were achieved with naftidrofuryl at a low dose (0.06 microM) and became more marked with naftidrofuryl at higher concentrations. In contrast, naftidrofuryl did not appear to modify routinely spontaneous platelet aggregation. These results show an in vitro antiaggregating effect of naftidrofuryl on platelets of aspirinized patients. However, the clinical interest of a such coadministration of naftidrofuryl and aspirin in patients, has still to be confirmed in a double blind randomized trial.

Aged↗
PubMed1992

Effects of teicoplanin on human platelet aggregation in vitro and ex vivo.

The effects of teicoplanin on adenosine-diphosphate (ADP)-induced human platelet aggregation in vitro and on both ADP- and ristocetin-induced human platelet aggregation ex vivo were investigated. In the in vitro study carried out on platelets from 7 healthy volunteers, teicoplanin had no effect on platelet function even at a concentration (1 mg/ml) 10 times higher than the peak level found in the in vivo state, but at the highest concentration (10 mg/ml), which is 100 times higher than that reached in vivo, it inhibited ADP-induced platelet aggregation. In the ex vivo studies carried out in 10 healthy volunteers, teicoplanin, following single intravenous doses of 400 mg and 800 mg, did not produce any effect on platelet function up to 6 hours after administration. After 12 hours, teicoplanin, when given at 800 mg i.v., reduced ADP-induced platelet aggregation.

Adult↗
PubMed2005

[Effect of phenolic alkaloids of Menispermum dauricum on thrombosis and platelet aggregation].

AIM: To observe the effect of phenolic alkaloids of Menispermum dauricum (PAMD) on thrombosis and platelet aggregation, and to explore its mechanism of action. METHODS: Thrombosis was observed with arteriovenous shunt thrombus model in rat; platelet aggregation was determined by Born's method; ultrastructure of platelet was observed by transmission electron microscope; TXB2 or 6-keto-PGF1alpha levels were assessed by radioimmunoassay; and NO was determined by colorimetric method. RESULTS: PAMD dose-dependently inhibited experimental thrombus formation, platelet aggregation induced by ADP, AA and THR in vivo and ultrastructure changes stimulated by THR; PAMD increased the generation of 6-keto-PGF1alpha in thoracic aortae and NO level in plasma; and had no influence on TXB2 release (P > 0.05). CONCLUSION: PAMD inhibited thrombosis and platelet aggregation, and its mechanism might be due to the increase of PGI2 and NO level.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

Circulating platelet aggregates induced by somatostatin in insulin-dependent diabetic subjects.

The present study was undertaken to reevaluate the influence of somatostatin on platelet function in insulin-dependent diabetics and in normal subjects. In in vivo studies, nine insulin-requiring diabetics were infused with cyclic somatostatin (250 microgram/hour) for 120 minutes or with saline, in randomized order. This dose of somatostatin, sufficient to depress the basal concentrations of plasma glucose, glucagon and C-peptide, resulted in no significant change of platelet aggregation response to either ADP or collagen. By contrast, a progressive and significant reduction of platelet aggregation response to ADP was found during saline infusion. A similar pattern of response was seen in normal subjects. In all diabetics, but not in normals, somatostatin induced the appearance of circulating platelet aggregates. In in vitro studies, somatostatin augmented the aggregation response to epinephrine in both normals and diabetics. In conclusion, somatostatin counteracts the decrease of platelet aggregation response to ADP seen in saline studies, induces the appearance of platelet aggregates in diabetics and potentiates the aggregation response to epinephrine (in vitro) in both normals and diabetics. These actions of somatostatin suggest some aggregating capacity of the peptide in man.

Adolescent↗
PubMed1990

A comparison of the effects of three positive inotropic agents (amrinone, milrinone and medorinone) on platelet aggregation in human whole blood.

Amrinone, milrinone and medorinone inhibit platelet aggregation in human whole blood. They are particularly potent inhibitors of arachidonic acid induced aggregation, inhibiting by 50% (IC50) at concentrations of 1.5 microM (milrinone), 7.5 microM (medorinone) and 48 microM (amrinone). Each drug was less potent at inhibiting ADP and collagen-induced aggregation. The rank order for inhibition of arachidonic acid - induced aggregation correlated well with the rank order of cyclic AMP phosphodiesterase inhibition for these drugs when compared to the response of a reference cAMP phosphodiesterase inhibitor (CI-930) and a reference cGMP phosphodiesterase inhibitor (M & B 22948). Since inhibition of platelet aggregation in vitro occurred at clinically relevant concentrations, it is evident that these agents have potentially beneficial antithrombotic properties.

Adenosine Diphosphate↗
PubMed1999

Comparison of the relative activities of alpha-tocopherol and PMC on platelet aggregation and antioxidative activity.

In this study, PMC (2,2,5,7,8-pentamethyl-6-hydroxychromane), a potent antioxidant derived from alpha-tocopherol, dose-dependently inhibited agonist-induced platelet aggregation in human platelet-rich plasma. PMC is over 5-10 times more potent than alpha-tocopherol in inhibiting human platelet aggregation. Moreover, PMC (25-350 microM) dose-dependently reduced the relative fluorescence intensity of platelet membrane tagged with diphenylhexatriene (DPH). PMC is about 6-times more potent than alpha-tocopherol on this effect. Furthermore, antioxidative activity of PMC was investigated using two in vitro models. PMC inhibited non-enzymatic iron-induced lipid peroxidation in rat brain homogenates with an IC50 value of 0.21+/-0.05 microM. It was more potent than alpha-tocopherol or other classical antioxidants. PMC also scavenged the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH). The concentration of PMC resulting in a decrease of 0.20 in the absorbance of DPPH was about 12.1+/-3.6 microM, was comparable in potency to alpha-tocopherol, butylated hydroxytoluence and Trolox. The antiplatelet activity of PMC may possibly be due initially to an increase in fluidity of the platelet membrane followed by inhibition of platelet aggregation. Our results indicate that PMC is a potentially effective antioxidant and antiaggregating agent, and could be helpful the design of compounds with more clinical effectiveness.

Animals↗
PubMed1992

[Effect of 3,4-dihydroxyacetophenone on platelet aggregation in normal pregnancy and pregnancy induced hypertension].

The effect of 3,4-Dihydroxyacetophenone (DHAP) on platelet aggregation in normal pregnancy and pregnancy induced hypertension (PIH) in the third-trimester was studied by optical method. The IC50 values of DHAP in inhibiting ADP-induced platelet aggregation in normal pregnancy and PIH were 1.0 x 10(-3) mol/L and 2.4 x 10(-3) mol/L respectively. A dose-effect relationship of DHAP was also demonstrated (r greater than 0.92). At various time-phases of ADP-induced platelet aggregation, the addition of DHAP to the platelet-rich plasma could rapidly decrease the two-phase aggregation. DHAP of 200-240 mg/d x 3-5 days by i.v. drips given to patients with PIH also inhibited ADP-induced platelet aggregation. The authors conclude that DHAP is a potent antithrombogenic agent both in vitro and in vivo and is therefore a promising drug to improve utero-placenta-fetal circulation.

Acetophenones↗
PubMed2004

Cilostazol and dipyridamole synergistically inhibit human platelet aggregation.

It has been previously shown that cilostazol (Pletal), a drug for relief of symptoms of intermittent claudication, potently inhibits cyclic nucleotide phosphodiesterase type 3 (PDE3) and moderately inhibits adenosine uptake. It elevates extracellular adenosine concentration, by inhibiting adenosine uptake, and combines with PDE3 inhibition to augment inhibition of platelet aggregation and vasodilation while attenuating positive chronotropic and inotropic effects on the heart. In the present study, we tested the hypothesis that cilostazol combined with a more potent adenosine uptake inhibitor, dipyridamole, synergistically inhibited platelet aggregation in human blood. In the presence of exogenous adenosine (1 microM), the combination of cilostazol and dipyridamole synergistically increased intra-platelet cAMP. Furthermore, cilostazol inhibited platelet aggregation in a washed platelet assay concentration-dependently with IC50s of 0.17 +/- 0.04 microM (P < 0.05 versus plus adenosine alone of 0.38 +/- 0.05 microM), 0.11 +/- 0.06 microM (P < 0.05), and 0.01 +/- 0.01 microM (P < 0.005) when combined with 1, 3, or 10 microM dipyridamole, respectively (n = 5). In whole blood, cilostazol (0.3 to 3 microM) and dipyridamole (1 or 3 microM) synergistically inhibited collagen- and ADP-induced platelet aggregation in vitro. Furthermore, the synergism was confirmed in an open-label, sequential study in healthy human subjects using ex vivo whole-blood collagen-induced platelet aggregation. Four hours after oral co-administration of cilostazol (100 mg) and dipyridamole (200 mg), platelet aggregation was inhibited by 45 +/- 17%, while no significant inhibition was observed from subjects treated with either drug alone. The combination may provide a potential treatment of arterial thrombotic disorders.

Adenosine↗
PubMed1991

[Platelet aggregation during hypotensive anesthesia using prostaglandin E1].

We studied platelet aggregation during hypotensive anesthesia using prostaglandin E1 (PGE1) on 22 patients (6 males, 16 female). All the patients underwent operations on head, neck, abdomen, breast, or lower extremities under general anesthesia. They had no history of hematological disease or taking drugs which affected platelet aggregation. The blood was sampled three times under a constant condition of anesthesia with intravenous drip: firstly, before using PGE1, secondly, under hypotensive state during PGE1 infusion at the speed of 0.05-0.3 micrograms.kg-1.min-1, and thirdly, after cessation of PGE1, after the blood pressure had recovered to the level before PGE1 infusion. ADP, collagen and epinephrine were added to the platelet rich plasma as clumping agents; their final concentrations were 0.3 microM, 2 micrograms.ml-1, and 2 micrograms.ml-1 respectively. The aggregating curves were recorded for 7 min. There were no significant differences in platelet aggregation among the three blood samples; neither in platelet count nor in bleeding time. Bleeding did not seem to have increased due to PGE1 infusion. These results suggest that PGE1 at hypotensive dose could be used safely under general anesthesia regarding hemostasis.

Adult↗
PubMed1982

Alpha-adrenergic stimulation of phosphatidylinositol synthesis in human platelets as an alpha-2 effect secondary to platelet aggregation.

Epinephrine and adenosine diphosphate (ADP) stimulated 3H-glycerol uptake into phosphatidylinositol of human platelets. Yohimbine, an alpha-2 adrenoceptor antagonist, markedly reduced epinephrine-stimulated 3H-glycerol uptake into phosphatidylinositol; while prazosin, an alpha-1 antagonist, was without effect. Likewise, yohimbine, but not prazosin, blocked epinephrine-induced platelet aggregation. Furthermore, clonidine, a specific agonist for alpha-2 adrenoceptors, stimulated incorporation of 3H-glycerol into phosphatidylinositol and promoted platelet aggregation in the presence of low concentrations of ADP. These studies indicate that the effects of epinephrine on platelet aggregation and phosphatidylinositol synthesis are mediated through alpha-2 adrenoceptors. Further, since the stimulation of phosphatidylinositol synthesis seen with epinephrine was also observed with ADP, this suggests that the increased 3H-glycerol labeling is an indirect result of platelet aggregation.

Adrenergic alpha-Agonists↗
PubMed2002

Aerosolized iloprost induces a mild but sustained inhibition of platelet aggregation.

Pathological studies have revealed that one of the main features encountered in the pulmonary vasculature of patients with pulmonary hypertension is the presence of thrombotic lesions. Open pilot studies have indicated that aerosolized iloprost may have beneficial effects in patients with pulmonary hypertension. The effects of aerosolized iloprost on platelet function and plasma cyclic adenosine monophosphate (cAMP) were studied. Platelet aggregation and plasma cAMP were measured at baseline, 30 min, 4 and 6 h after inhalation of 15 microg iloprost in 10 healthy volunteers. Maximal platelet aggregation in response to adenosine diphosphate (ADP) (2 and 6 micromol x L(-1)), collagen (2.5 and 5 microg x mL(-1)), epinephrine (1.25 and 5 micromol x L(-1)) and arachidonic acid (0.5 mg x mL(-1)) was measured. Platelet aggregation was significantly inhibited at 30 min in response to ADP (2 and 6 micromol x L(-1), epinephrine (1.25 and 5 micromol x L(-1)) and collagen (2.5 microg x mL(-1)). It was still inhibited at 4 h in response to the same agents, but normalized at 6 h. cAMP increased at 30 min, from 27.3+/-1.2 to 31.8+/-1.2 nmol x L(-1), remained increased at 4 h (29.2+/-1.3 nmol x L(-1)) and normalized at 6 h (27.4+/-1.1 nmol x L(-1)). Aerosolized iloprost induced a mild but sustained inhibition of platelet aggregation. Platelet aggregation inhibition may be one of the mechanisms which explains the beneficial effect of repeated inhalation of iloprost in pulmonary hypertension.

Administration, Inhalation↗