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 811 records · Page 45Linked to original sources
PubMed1993

Inhibitory effects of S-(1,2-dicarboxyethyl)glutathione on collagen-induced platelet aggregation; enhancements of cyclic AMP level and adenylate cyclase activity in platelets by S-(1,2-dicarboxyethyl)glutathione.

S-(1,2-Dicarboxyethyl)glutathione (DCE-GS) in addition to being present in the liver, lens, and heart, also inhibited platelet aggregation. To clarify these inhibitory effects, the role of DCE-GS in the release of ATP and serotonin from platelets was studied, as was thromoboxane A2 formation, cyclic AMP level and adenylate cyclase activity in human platelets. The results are as follows: DCE-GS at a concentration of 1.3 mM inhibited ATP and serotonin release from platelets induced by collagen, by 77.4 +/- 4.3 and 78.7 +/- 6.3%, respectively. At 1.5 mM DCE-GS also inhibited the formation of thromboxane B2 by 79.6 +/- 4.1%. Incubation of human platelet rich plasma with 2 mM of DCE-GS for 10 min increased the cyclic AMP level and the activity of adenylate cyclase by 204 +/- 28 and 211 +/- 11.7%, respectively. These results suggest that the inhibitory effect of DCE-GS on the platelet aggregation induced by collagen is due to an increase in the cyclic AMP level in platelets, which in turn may be due to enhancement of the activity of adenylate cyclase.

Adenosine Triphosphate↗
PubMed1985

Inhibition of platelet aggregation by synthetic phosphatidylcholines: possible involvement of vesiculation of platelet plasma membranes.

Synthetic phosphatidylcholines inhibited thrombin-induced aggregation of rabbit platelets. The inhibitory effect of the phosphatidylcholines increased with an increase in the chain-length of the constituent fatty acids up to 12, and then decreased, and C14:0PC and C16:0PC did not inhibit platelet aggregation. The activity of synthetic phosphatidylcholines as to induction of vesiculation of platelet plasma membranes (Kobayashi, T., Okamoto, H., Yamada, J.-I., Setaka, M. and Kwan, T. (1984) Biochim. Biophys. Acta 778, 210-218) and the inhibitory effect of these phosphatidylcholines on platelet aggregation showed the same dependence on the constituent fatty acids of the phosphatidylcholines. The amounts of phosphatidylcholines required for 50% inhibition of platelet aggregation correspond very well to those required for 15% exfoliation of acetylcholinesterase activity, suggesting that there is a close relationship between platelet aggregation and vesiculation of the platelet plasma membrane. The possible mechanism of inhibition of platelet aggregation by synthetic phosphatidylcholines is discussed.

Acetylcholinesterase↗
PubMed1981

Platelet aggregation in patients with Moyamoya disease.

Platelet aggregation was studied by giving ADP or adrenalin to 28 patients with Moyamoya disease. There were 7 males and 21 females, and 27 normal controls, 11 males and 16 females. We found that 2 muM of ADP, and 9.1 and 22.7 muM of adrenalin induced statistically significant increases in nondissociative patterns of platelet aggregation in the patient group. Maximum aggregation was significantly increased in the patient group compared with the controls by the addition of ADP (2 and 4 muM) or adrenalin (9.1 and 22.7 muM). When patients were divided into two groups under and over 20 years of age, there was no discernible difference of platelet aggregation in either group.

Adenosine Diphosphate↗
PubMed2003

Anti-inflammatory and anti-platelet aggregation activity of human placental extract.

AIM: To find the anti-inflammatory and anti-platelet aggregatory activity of human placental extract (HPE, Placentrex). METHODS: The HPE was studied for anti-inflammatory effect in Wistar rats on carrageenin, serotonin (5-HT), and prostaglandin E1 (PGE1) induced edema in acute model and cotton pellet induced granuloma on sub-acute model. Anti-platelet aggregation was studied against protection of adinosine diphosphate (ADP)-induced aggregation of human platelet through in vitro study. RESULTS: HPE showed positive results both in acute and sub-acute models of inflammation. Highly significant (P<0.01) results were obtained against 5-HT induced acute inflammation and cotton pellet induced sub-acute inflammation in comparison with standard (diclofenac sodium) and control (normal saline) drugs. The anti-inflammatory property of HPE in animal model was well supported with clinical study of platelet aggregation. There was highly significant (P<0.01) inhibition of platelet aggregation with HPE at different doses against ADP. CONCLUSION: Our data suggest that human placental extract may be useful in suppressing inflammation and platelet aggregation.

Animals↗
PubMed1982

SIN-1, the main metabolite of molsidomine, inhibits prostaglandin endoperoxide analogue- and arachidonic acid-induced platelet aggregation as well as platelet thromboxane A2 formation.

N-Carboxy-3-morpholinosydnone imine ethyl ester (molsidomine) and its main metabolite 3-morpholinosydnone imine (SIN-1) were investigated in rabbit platelet-rich plasma (PRP) for antiaggregatory activity and inhibition of thromboxane A2 (TXA2) generation (arachidonic acid (AA)-induced) as well as in human PRP regarding prostaglandin endoperoxide analogue (U-46 619)- and AA-induced aggregation and TXB2 formation. The results were compared with the effects of nictindole. In rabbit PRP the inhibitory effects of molsidomine on aggregation and TXA2 generation were 20fold lower than that of SIN-1. The IC50-values of SIN-1, which is the pharmacologically active biotransformation product of molsidomine, were about 1 mumol/l in the experimental models used. The inhibitory effects of nictindole were about 50 times higher than those of SIN-1. In human PRP the inhibitory potency of SIN-1 decreased in the following sequence: U-46 619-induced aggregation (IC50 = 0.9 mumol/l) greater than AA-induced aggregation (IC50 = 1.4 mumol/l) greater than TXB2 formation (IC50 = 2.9 mumol/l). Molsidomine was nearly without effect in human PRP. Our own preliminary results and findings obtained by other authors seem to exclude a direct effect of SIN-1 on cyclooxygenase and thromboxane synthetase. The possible clinical significance of our findings in different types of angina pectoris and for myocardial infarction is discussed.

Animals↗
PubMed1994

Shear-induced platelet aggregation in cerebral ischemia.

BACKGROUND AND PURPOSE: Recent evidence has suggested that shear-induced platelet aggregation is an important mechanism of thrombosis at arterial bifurcations or stenoses. We measured shear-induced platelet aggregation with a new apparatus in patients with cerebral ischemia and also studied correlations with other hemostatic parameters as well as the effect of antiplatelet agents. METHODS: The subjects were 75 patients with cerebral ischemia and 26 control subjects. Platelet aggregation was induced in citrated platelet-rich plasma by a high shear stress (108 dynes/cm2) that was applied by means of a cone-plate streaming chamber based on turbidimetry. We studied the correlation of test results with hemostatic parameters and also the effects of antiplatelet agents. RESULTS: Compared with the control subjects, an increase of shear-induced platelet aggregation was observed in 21 patients with atherothrombotic stroke and 12 with transient ischemic attacks, but not in 11 with cardioembolic stroke or 31 with lacunar stroke. There was no significant correlation of shear-induced platelet aggregation with platelet count, agonist-induced platelet aggregation, fibrinogen level, or beta-thromboglobulin level. The extent of shear-induced aggregation was not correlated with von Willebrand factor antigen levels but was significantly correlated with the amounts of larger von Willebrand factor multimers. Oral aspirin (81 mg/d) did not inhibit shear-induced platelet aggregation, whereas oral ticlopidine (200 mg/d) significantly inhibited it. CONCLUSIONS: These results indicate that shear-induced platelet aggregation is increased in patients with atherothrombotic stroke and transient ischemic attacks, is correlated with the increase of larger von Willebrand factor multimers, and is corrected by ticlopidine but not by low-dose aspirin.

Adult↗
PubMed1982

Platelet aggregation in whole blood determined using the Ultra-Flo 100 Platelet Counter.

The Ultra-Flo 100 Whole Blood Platelet Counter has proved a useful tool for measuring platelet aggregation in whole blood, the extent of aggregation being deduced from the number of single platelets that remain. The technique has allowed us to show that platelets aggregate spontaneously in citrated blood and in heparinized blood but not in whole blood collected into EDTA. The aggregation occurs during storage but its rate is enhanced by stirring and it occurs more readily when the whole blood has been exposed to plastic rather than glass. It occurs much more readily in whole blood from some individuals than from others and the process may involve adenosine diphosphate (ADP). The rate of aggregation in whole blood is enhanced by several aggregating agents including collagen, ADP and sodium arachidonate which are more usually studied in platelet-rich plasma.

Adenosine Diphosphate↗
PubMed1989

Histamine is an intracellular messenger mediating platelet aggregation.

Inhibition of human platelet aggregation by N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine-HCl (DPPE), a novel antagonist of histamine binding, suggested that histamine might serve a critical role in cell function. Phorbol-12-myristate-13-acetate (PMA) or collagen was found to increase platelet histamine content in parallel with promotion of aggregation. Inhibitors of histidine decarboxylase (HDC) suppressed both aggregation and the elevation of histamine content, whereas DPPE inhibited aggregation only. In saponin-permeabilized platelets, added histamine reversed the inhibition by DPPE or HDC inhibitors on aggregation induced by PMA or collagen. The results indicate a role for histamine as an intracellular messenger, which in platelets promotes aggregation.

Blood Platelets↗
PubMed1983

Platelet aggregation studies in whole human blood.

Since the development of the photometric aggregometer, platelet aggregation studies are routinely performed on platelet-rich plasma (PRP). We have studied platelet aggregation in fresh citrated whole human blood using the recently developed Ultra Flo 100 Whole Blood Platelet Counter. Aggregation of platelets in whole blood was induced with adenosine 5'-diphosphate (ADP; 0.25-10 microM), collagen (0.25-1.0 microgram/ml) and thrombin (0.05-0.2U/ml). Platelet aggregation induced by ADP and thrombin was maximum within 1 min, and that of collagen within 3 mins. Aggregation responses to low concentration of ADP and thrombin were rapidly reversible, whereas responses to collagen and high concentrations of ADP and thrombin were virtually irreversible. The aggregation of platelets was indicated by a fall in platelet count; confirmed by scanning electron micrographs which revealed the presence of large aggregates of platelets, and was prevented when blood was treated with EDTA as anticoagulant. The present technique appears to be rapid, sensitive and reliable; and allows direct measurement of platelet aggregation and disaggregation in whole blood in vitro and ex-vivo.

Adenosine Diphosphate↗
PubMed1996

Inhibition of collagen-induced platelet aggregation in Japanese black cattle with inherited platelet disorder, Chediak-Higashi syndrome.

Aggregation properties of platelets were examined in Japanese Black cattle with Chediak-Higashi syndrome (CHS) and normal control cattle. Platelet aggregation induced by collagen was decreased in platelets of the cattle with CHS, but not ADP (10-20 microM), thrombin (0.5-1.0 U/ml) and phorbol-12-myristate 13-acetate (PMA, 3.2 microM). The aggregation response induced by collagen in CHS platelets lacks the change in shape which usually occurs in normal platelets. Simultaneous stimulation by collagen (10 micrograms/ml) + ADP (10 microM) is effective in restoring collagen-induced aggregating response in CHS platelet, although pretreatment of ADP (10 microM) could not restore the collagen (10 micrograms/ml)-induced aggregating response, suggesting that there is a certain threshold of stimulation intensity above which collagen-induced aggregation of CHS platelet can begin. Control normal platelets, previously exposed to ADP (10 microM) and collagen (10 micrograms/ml), showed no further response to exposure to a third aggregating agent (arachidonic acid, 5 mM). On the other hand, the final agent was able to elicit aggregating responses in CHS platelets, suggesting that the arachidonate aggregating system may be suppressed in CHS cattle, but fully activated in control animals. Furthermore, normal platelets showed a significant decrease in aggregating response to collagen when pretreated with a cyclooxygenase inhibitor, indomethacin (10(-5) M), whereas CHS platelet was insensitive to indomethacin. This indomethacin-treated normal platelet mimicked the CHS collagen-induced aggregation pattern. These data suggest that a signal transduction process from receptor-operated events to arachidonate metabolism is suppressed in collagen-induced CHS platelet aggregation.

Adenosine Diphosphate↗
PubMed1993

Decreased platelet aggregation during pregnancy correlates with gestational age.

In vivo platelet aggregation was determined in pregnant women at different gestational ages and nonpregnant women by a modification of a method. A higher platelet count ratio (PCR) was found in pregnant women after a gestational age of 13 weeks. At 16-30 and 31-41 weeks of gestation, in vivo platelet aggregation was significantly decreased. The PCR, meaning the ratio of non-aggregated platelets to all circulating platelets, correlated significantly with gestational age. It is suggested that the decrease in in vivo aggregation measured during pregnancy reflects a summarized effect of different factors during pregnancy connected to placenta and uteroplacental vessels.

Adolescent↗
PubMed1990

Aggregating platelets increase intracellular calcium in endothelial cells through release of adenine nucleotides.

Aggregating platelets relax isolated coronary arteries through the release of endothelium-derived relaxing factor (EDRF). Since release of EDRF may be calcium dependent, we tested if and how aggregating platelets stimulated a calcium response in cultured endothelial cells. Aggregating platelets caused a transient increase in intracellular calcium in endothelial cells loaded with the fluorescent calcium indicator fura-2. The adenine nucleotides ADP and ATP, but not other platelet-derived mediators, mimicked the platelet-induced calcium response, and inhibition of adenine nucleotides impaired the response to aggregating platelets. Thus, aggregating platelets release adenine nucleotides and stimulate a rise in intracellular calcium in cultured endothelial cells. This calcium response may represent the intracellular transduction mechanism by which aggregating platelets induce endothelial release of EDRF and subsequent relaxation of coronary arteries.

Adenine Nucleotides↗
PubMed1975

Blood platelet aggregation and personality traits.

Changes in blood platelet aggregation may precipitate episodes of arterial occlusive diseases. Little is known, however, regarding the influence of psychological traits, emotional states and other behavioral stressors on platelet aggregation phenomena. This study examined 46 healthy college men at rest and after submaximal treadmill exercise. Associations were found between the duration of platelet aggregation and a number of scores from the California Psychological Inventory and self-administered anxiety scales. The more socially adequate, poised and dominant persons--those with more mature ego development and less overt anxiety--had platelets with more prolonged aggregation reactions to the in vitro introduction of noradrenalin. Irreversible aggregation of platelets occurred more regularly to lower in vitro concentrations of noradrenalin in platelet samples drawn from subjects who were less anxious and tended to be more rigidly defensive. It is premature to attempt to derive clinical implications from this exploratory work, but some implications for the design of future research are discussed.

Adult↗
PubMedDate not supplied

Inhibition of platelet aggregation by putrescine, spermidine, and spermine in hypercholesterolemic rabbits.

BACKGROUND: Hypercholesterolemia causes alterations in platelet function. Platelet hyperaggregation is considered a predisposing factor for atherosclerosis. In this paper, the antiaggregating effect of the polyamines putrescine, spermidine, and spermine was studied on platelets of normal and hypercholesterolemic rabbits. METHODS: New Zealand rabbits were fed with a cholesterol-enriched diet for 10 weeks. Lipids and glucose were determined in serum. The assays of platelet aggregation were carried out using platelet-rich plasma (PRP) obtained from both control and cholesterol-fed rabbits. We used 2.5 micromol /mL ADP and 2 microg/mL collagen as inductors of platelet aggregation. In addition, arginase activity and L-arginine content were determined in PRP. RESULTS: Serum total cholesterol and LDL-cholesterol concentrations were increased from 26.3 +/- 8.1 to 1,485.0 +/- 26.8 mg/dL and from 15.9 +/- 5.9 to 1,383.8 +/- 58.9 mg/dL, respectively, whereas triglyceride concentration increased from 88.3 +/- 35.6 to 411.0 +/- 154.5 mg/dL upon cholesterol feeding. Seventy-five percent of platelet aggregation inhibition was observed with 10 microM of polyamines in PRP of normal rabbits. Spermine inhibited platelet aggregation by 54% in PRP of hypercholesterolemic rabbits when ADP was used as agonist. The order of polyamine action was spermine > spermidine > putrescine. In addition, we found that platelet arginase activity and L-arginine content were unaltered upon hypercholesterolemia. CONCLUSIONS: These results show that the polyamines putrescine, spermidine, and spermine have antagonist action in platelet aggregation and suggest a key role of polyamines in platelet aggregation under normal and hypercholesterolemic conditions.

Animals↗
PubMed1980

The effects of vincristine on platelet aggregation studied by a filter loop technique in the rat.

1 A method for measuring aggregation of platelets of adenosine diphosphate (ADP) is described using a filter inserted into the flowing aortic blood in the rat. 2 Repeated infusions of ADP resulted in a fall in the calculated aggregation index without significant changes in the platelet count. 3 Vincristine (0.05 mg/kg) intravenously caused significant inhibition of ADP-induced platelet aggregation. 4 Infusion of ADP caused some peripheral vasodilatation though it is unlikely that this contributed to the effects seen to any great extent.

Adenosine Diphosphate↗
PubMed1997

Alteration of platelet aggregation in patients with thyroid disorders.

To determine whether Graves' disease or primary hypothyroidism influence platelet function, we evaluated platelet aggregation in the platelet-rich plasma (PRP) from such patients. Platelet aggregation induced by adenosine diphosphate (ADP) in blood obtained from patients with untreated Graves' disease was significantly lower than normal, whereas that in patients with untreated primary hypothyroidism was relatively increased. The magnitude of platelet aggregation induced by collagen in both groups of patients resembled that induced by ADP. However, significant differences were evident between the two diseases (P < .05). In addition, we observed a significant inverse correlation between the extent of platelet aggregation and plasma levels of thyroid hormones (triiodothyronine [T3], thyroxine [T4], and free T3). Platelet aggregation returned to normal when the euthyroid condition was obtained in the patients following administration of antithyroid drugs or thyroid hormone. The findings are consistent with the possibility that thyroid hormones influence platelet aggregation partly via inhibition of myosin light-chain kinase (MLCK).

Adenosine Diphosphate↗
PubMed1991

Effect of fibrinogen concentration on the velocity of platelet aggregation.

The relationship between fibrinogen binding to its receptor and platelet aggregation has been investigated by comparing 125I-fibrinogen binding and aggregation velocities of gel-filtered platelets in the presence of adenosine diphosphate (ADP). Aggregometric responses at various fibrinogen concentrations are found to be bell-shaped and show a maximum at fibrinogen concentrations (Fmax) similar to the 125I-fibrinogen hemisaturating doses. At higher and lower fibrinogen concentrations, platelet aggregation velocities decrease in a parallel manner. Lowering ADP concentration increases Fmax, in agreement with the modulatory effect of ADP on fibrinogen binding to platelets. Variations of fibrinogen in the range of physiopathologic plasma concentrations affect platelet aggregation induced by any ADP dose. These results clarify the relationship between the fibrinogen binding process and aggregation and demonstrate that plasma fibrinogen concentration has a major influence on the velocity of platelet aggregation.

Adenosine Diphosphate↗
PubMed1995

[Effect of controlled hypotension using sodium nitroprusside on platelet aggregation].

OBJECTIVE: To determine the influence of sodium nitroprusside (SNP) on platelet aggregation when this agent is used to induce hypotension during surgery. PATIENTS AND METHODS: Spontaneous platelet aggregation (SPA) determined by impedance measurement and induced platelet aggregation (IPA) determined by turbidimetry were studied in 30 subjects scheduled for elective ear, nose or throat surgery. Fifteen patients in the SNP group (SNPG) received SNP in doses adjusted to maintain a mean arterial pressure of 50 mmHg. Another 15 patients who did not receive SNP served as controls. RESULTS: SPA increased progressively in both groups. The greatest increase occurred after anesthetic induction (control group +172%, SNPG +48%); the highest level recorded was reached on the morning of the first day after surgery (control group +215%, SNPG +46%). IPA decreased after anesthetic induction (control group -21%, SNPG -40%) and stayed down throughout surgery. IPA was higher on the first morning after surgery than before the operation (control group +35%, SNPG +2%). SPA was significantly higher 60 minutes after start of surgery than before surgery in the control group; IPA and SPA were likewise higher in these patients the morning after surgery. CONCLUSIONS: Platelet aggregation increases during surgery and in the immediate postoperative period. This increase is attenuated when SPA is given to induce hypotension. SPA should be determined by measurement of impedance in whole blood when the nature of platelet aggregation during surgery is being studied, given that early increases in IPA can be masked as a result of the low sensitivity of turbidimetry.

Blood Coagulation Disorders↗