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PubMed1990

Experimental and clinical studies on inhibitory effect of ganoderma lucidum on platelet aggregation.

In this study we observed the inhibitory effect of Chinese herbal medicine Ganoderma lucidum (GL) on platelet aggregation in 15 healthy volunteers and 33 patients with atherosclerotic diseases. The results showed that the first and the second phase of aggregation of platelets of the healthy volunteers were obviously inhibited (P less than 0.01) when watery soluble extract of GL of different concentrations was added to the platelets in vitro, i. e., the reaction speed of platelet aggregation was slowed down. The inhibitory effect was related to dosage. Platelet aggregation induced by ADP in final concentration of 2 mumol/L and 3 mumol/L was obviously inhibited, after the patients had taken GL 1 g 3 times a day for 2 weeks, the maximum platelet aggregation inhibition rates were then 31.49% (P less than 0.01) and 17.7% (P less than 0.01) respectively. Length and weights (wet and dry) of the extracorporeal thrombi were reduced from 30.05 +/- 4.38 mm, 103.9 +/- 9.33 mg and 44.89 +/- 4.79 mg to 20.4 +/- 2.33 mm (P less than 0.05), 85.27 +/- 8.77 mg (P less than 0.01) and 35.1 +/- 4.5 mg (P less than 0.01) respectively after oral administration of GL. The results of our experiments suggested that the Chinese herbal medicine GL may be an effective inhibitory agent of platelet aggregation. However, its mechanism and active principles remain to be further investigated.

Aged↗
PubMedDate not supplied

Suppressive effect of captopril on platelet aggregation in essential hypertension.

Effects of captopril on platelet aggregation were studied in 12 essential hypertensive subjects. At the same time, the effects of captopril and angiotensin II on platelet aggregation in vitro were examined in 20 volunteers. A 50-mg oral dose of captopril was administered daily to hypertensive subjects for 2 weeks; the dose was then increased to 100 mg daily for the next 2 weeks. Values of platelet aggregation induced by ADP, epinephrine, collagen, and arachidonic acid before captopril treatment were 71.9 +/- 4.5, 77.3 +/- 4.2, 72.4 +/- 4.1, and 70.8 +/- 4.3% (mean +/- SE), respectively. Two weeks after daily administration of 50 mg captopril, these values were 56.7 +/- 4.5, 50.8 +/- 7.6, 64.0 +/- 4.6, and 60.9 +/- 3.9%, respectively, with significant reduction of platelet aggregation (p less than 0.001, p less than 0.01, p less than 0.01, and p less than 0.005, respectively). Daily administration of 100 mg captopril also had a significant suppressive effect on platelet aggregation. Changes of platelet count and serum lipids were not significant. In vitro, captopril and angiotensin II added to platelet-rich plasma had no effect on platelet aggregation. These results show that the suppressive effect of captopril on platelet aggregation is a secondary action in vivo.

Aged↗
PubMed1979

[Changes in platelet aggregation and fibrinolytic activity of blood in healthy persons during the 23-day physical cycle].

The blood of 100 health humans aged 18 to 40 years was analysed. The aggregation of platelets and blood fibrinolytic activity were shown to change within 23-day physical cycle according to Swoboda and Fliess. In the negative phase the platelets count, their aggregation, desaggregation process and blood fibrinolytic activity were higher than in the positive one. No substantial differences in platelets aggregation and blood fibrinolytic activity were found during the positive and negative phases of the emotional or intellectual cycles.

Activities of Daily Living↗
PubMed1991

Platelet-activating factor (PAF) receptor antagonists inhibit arachidonic acid induced platelet aggregation in rabbit whole blood.

The potency of several platelet-activating factor (PAF) receptor antagonists was measured by observing their inhibitory effects against PAF induced platelet aggregation. Their selectivity was assessed by monitoring their effect on platelet aggregation induced by arachidonic acid (AA) and adenosine diphosphate (ADP). The antagonists inhibited platelet aggregation induced at the PAF EC50 (0.023 microM) with the following rank order of potency: WEB 2086 greater than WEB 2170 greater than SRI 64-412 greater than SRI 63-675 greater than BN 52021 greater than kadsurenone greater than SRI 63-441 greater than alprazolam. While the antagonists had no inhibitory effect at the EC50 for ADP (10 microM), they did inhibit platelet aggregation induced at the EC50 for AA (55 microM). However, there was considerable variability in the slope of the inhibitory response and the relative potency of each antagonist against PAF induced platelet aggregation as compared to AA induced platelet aggregation. The antagonist IC50 (microM) against PAF and AA were as follows, with those that showed significantly different (p less than 0.01) slopes indicated by an asterisk: SRI 63-441* (3.8, 15.1); SRI 63-675 (1.4, 36.2); SRI 64-412 (0.5, 10.5); BN 52021* (2.4, 58.9); kadsurenone* (2.8, 28.3); alprazolam* (10, 25); WEB 2086 (0.055, 0.220), and WEB 2170 (0.107, 0.534). Therefore, in rabbit whole blood the antagonists were potent, although not completely selective, inhibitors of PAF induced platelet aggregation. These results suggest that the mode of action of PAF and AA induced platelet aggregation may share some common features. However, since the slope of the inhibitory response against PAF and AA for some antagonists differed, mechanistic differences in their action appear to exist.

Adenosine Diphosphate↗
PubMed1987

The role of platelet cyclooxygenase and lipoxygenase pathways in tumor cell induced platelet aggregation.

Walker 256 carcinosarcoma cells induce the aggregation of rat platelets and concomitant production of eicosanoid metabolites (e.g., 12-hydroxyeicosatetraenoic acid, thromboxane A2). Cyclooxygenase inhibitors, but not lipoxygenase inhibitors, were able to inhibit platelet aggregation induced in vitro by low concentrations of agonists. At high agonist concentrations, neither cyclooxygenase nor lipoxygenase inhibitors affected platelet aggregation; however the combination of both inhibitors resulted in inhibition of aggregation. Also, a low concentration of agonist induced minimal eicosanoid metabolism, whereas a high concentration resulted in increased eicosanoid metabolism. These inhibitors, at the doses tested, did not inhibit protein kinase C activity.

Animals↗
PubMed1986

A critical investigation into the existence of circulating platelet aggregates.

By a method of counting single platelets in diluted whole blood, platelet aggregates were quantified ex-vivo. Four groups: 20 thrombotic patients, 10 non-thrombotic patients, 10 healthy old controls and 10 healthy young controls were included in the study. Using a 19 gauge needle, with and without tubing, venous blood was taken into buffered EDTA, as a disaggregating agent and buffered EDTA-formalin, as the fixative. The amount of platelet aggregates quantified was affected by the quality of venepuncture or the rate of blood flow through the needle, but was unaffected by the presence of the tubing. There was no statistically significant difference between the four groups, in terms of the platelet aggregates quantified, but scanning electron microscopy revealed the presence of irreversible aggregates, composed of platelet red and white blood cells, in the blood of a greater number of thrombotic patients than non-thrombotic or healthy controls. Platelet aggregates were also quantified in aliquots of platelet rich plasma, and were found to be significantly greater than the corresponding values in whole blood. The difference appeared to be due to increased viscosity of the plasma, induced by the fixative which reduces platelet mobility during centrifugation. It is concluded that the platelet aggregates which disaggregate in buffered EDTA may represent an artifact of blood collection; the irreversible aggregates are suspected to represent the in vivo circulating aggregates.

Adult↗
PubMed1980

Selective deficiency in collagen-induced platelet aggregation during L-asparaginase therapy.

Platelet aggregation studies were performed on 10 pediatric patients with acute lymphoblastic leukemia (ALL) receiving induction therapy with vincristine, prednisone, and L-asparaginase. An isolated abnormality in platelet aggregation in response to collagen was found in all patients during the course of therapy. Platelet aggregation in response to collagen normalized following the discontinuation of L-asparaginase, while patients were still on vincristine and prednisone. In contrast to the abnormal collagen response, platelet aggregation induced by epinephrine, arachidonic acid, adenosine diphosphate (ADP), and thrombin were normal both during and following therapy. In the one patient with a normal platelet count before therapy, aggregation induced by all agents was normal. This selective abnormality in collagen aggregation therefore appears to result from therapy, with the use of L-asparaginase in particular being implicated.

Asparaginase↗
PubMed1987

Platelet-collagen adhesion enhances platelet aggregation induced by binding of VWF to platelets.

Ristocetin-induced platelet aggregation (RIPA) was evaluated in the presence of platelet-collagen adhesion. RIPA of normal donor platelet-rich plasma (PRP) demonstrated a primary wave of aggregation mediated by the binding of von Willebrand factor (VWF) to platelets and a secondary aggregation wave, due to a platelet-release reaction, initiated by VWF-platelet binding and inhibitable by acetylsalicylic acid (ASA). An enhanced RIPA was observed in PRP samples to which collagen had been previously added. These subthreshold concentrations of collagen, which by themselves were insufficient to induce aggregation, caused measurable platelet-collagen adhesion. Subthreshold collagen did not cause microplatelet aggregation, platelet release of [3H]serotonin, or alter the dose-responsive binding of 125I-labeled VWF to platelets, which occurred with increasing ristocetin concentrations. However, ASA inhibition of the platelet release reaction prevented collagen-enhanced RIPA. These results demonstrate that platelet-collagen adhesion altered the platelet-release reaction induced by the binding of VWF to platelets causing a platelet-release reaction at a level of VWF-platelet binding not normally initiating a secondary aggregation. These findings suggest that platelet-collagen adhesion enhances platelet function mediated by VWF.

Blood Platelets↗
PubMed1981

A physiologic regulator of collagen-induced platelet aggregation: inhibition by Clq.

Platelet aggregations were studied by a turbidimetric method in citrated human platelet-rich plasmas (PRP) in vitro. Human Clq inhibited the aggregations caused by collagens derived from different tissues and species. Clq was needed by weight in comparable quantities to collagen for neutralizing the aggregating effect. The dependence of the inhibitory reaction on the preincubation of platelets with CLq and the differences in the occurrence of aggregating substances in supernatants of PRP triggered with collagen in the presence or absence of Clq, confirmed that Clq exerts its effect by preventing fixation of collagen to platelets. In addition, the high specificity of the inhibitory action of Clq for collagen-induced platelet aggregation was demonstrated by results obtained for testing a variety of aggregating agents in combination with Clq and/or collagen. Since normal concentrations of Clq in the blood are in the range of inhibitory doses of Clq for collagen-induced platelet aggregations in vitro and upon activation of complement Clq is known to dissociate from Cl, it is proposed that Clq may participate in a highly specific manner in regulating platelet reactivity in collagen in vivo.

Animals↗
PubMed1984

Serum albumin enhances the impairment of platelet aggregation with thromboxane synthase inhibition by increasing the formation of prostaglandin D2.

Dazoxiben, a thromboxane synthase inhibitor, inhibits arachidonic acid induced aggregation in platelet-rich plasma from some donors only ("responders"). We have studied the effect of dazoxiben in vitro on platelet aggregation and prostaglandin (PG) metabolism and the influence of the incubation period and of exogenously added serum albumin (SA). SA, which increases the production of anti-aggregatory PGD2 from cyclic endoperoxides, induced "non-responder" human platelets to respond. With rabbit platelets, however, that are insensitive to PGD2, exogenous SA failed to potentiate dazoxiben-induced inhibition. The ratio between PGD2 and TXB2 + PGE2 formed was crucial in determining the response of human platelets to dazoxiben: whenever this ratio was high, platelet aggregation was inhibited. SQ 22536, an adenylate cyclase inhibitor, and NO164, a PGD2 antagonist, reversed the inhibition by dazoxiben in human platelet-rich plasma, stressing the importance of a PGD2 mediated rise of cyclic AMP for the effectiveness of a thromboxane synthase inhibitor.

Adenine↗
PubMed1996

Agonist-induced actin polymerization is required for the irreversibility of platelet aggregation.

Cytochalasin D was used to investigate the role of intracellular cytoskeleton in the stabilization of platelet aggregation induced by strong platelet agonists. Incubation of gel-filtered platelets with increasing concentrations of cytochalasin D resulted in a dose-dependent inhibition of actin polymerization and association of actin-binding proteins with the Triton X-100-insoluble material induced by the thromboxane analogue, U46619, and the thrombin receptor activating peptide, TRAP. The same concentrations of cytochalasin D did not significantly inhibit platelet aggregation promoted by the two agonists. The addition of the chelating agent EDTA to fully aggregated platelets, that had been treated with cytochalasin D, resulted in the rapid and almost complete disaggregation. EDTA did not cause disaggregation of control, solvent-treated, aggregated platelets. The degree of platelet disaggregation induced by EDTA was dependent on the dose of cytochalasin D used, and was correlated with the inhibition of the cytoskeletal reorganization. Aggregation of cytochalasin D-treated platelets stimulated with U46619 or TRAP was also reverted by the addition of the tetrapeptide RGDS or the fibrinogen gamma-chain dodecapeptide, which competitively interfere with fibrinogen binding to the glycoprotein IIb-IIIa complex. These results indicate that the intracellular cytoskeleton plays an essential role in the stabilization of the fibrinogen-platelet interaction, and is necessary for the irreversibility of platelet aggregation induced by strong agonists.

Actins↗
PubMed1984

Tumor-cell-platelet aggregation does not correlate with metastatic potential of rat 13762NF mammary adenocarcinoma tumor cell clones.

The ability of tumor cells to induce platelet aggregation has been correlated with their capacities to colonize the lungs of experimental animals. We tested this hypothesis by studying the ability of cloned, low-passage metastatic tumor cell lines derived from rat 13762NF mammary adenocarcinoma to aggregate rat platelets in vitro and in vivo, and we then compared this activity to metastatic potential by determining the incidence of lung metastasis after subcutaneous or intravenous inoculation of the tumor cell clones into syngeneic rats. Our results failed to show a correlation between in vitro platelet-aggregating activity and metastatic potential. In this system we could not detect platelet-aggregation activity with the most metastatic tumor clone, while least metastatic clone clearly possessed high platelet-aggregating activity. In addition, by measuring changes in blood platelet and fibrinogen concentrations at various intervals following intravenous injection of tumor cell clones, we were able to confirm in vivo the observed in vitro differences in their platelet-aggregating activities. Thus, platelet aggregating activity is heterogeneously expressed among 13762NF cell clones and appears unrelated to spontaneous or experimental metastasis in this tumor system.

Adenocarcinoma↗
PubMed1995

[Effect of acetylsalicylic acid on platelet aggregation and capillary bleeding in healthy cats].

The influence of acetylsalicylic acid (ASA) in vitro and in vivo on several parameters of the hemostatic system was evaluated in healthy cats. The aggregation response of cat platelets in vitro was not influenced by 10 micrograms ASA/ml plasma, whereas ASA concentrations of 35, 70, 100 micrograms/ml and of 1 mg/ml consistently inhibited the platelet aggregation induced by 0.1 (n = 4 cats) and 0.25 micrograms collagen/ml (n = 6 cats). The aggregation response to ADP and thrombin was partially (n = 2) or completely (n = 8) inhibited by an ASA concentration of 5 mg/ml. Administration of ASA at a dosage of 10 and 25 mg/kg BW orally and intravenously yielded a plasma concentration of salicylic acid of 30-42 micrograms/ml (10 mg/kg BW) and 50-70 micrograms/ml (25 mg/kg BW). All the dosages of ASA produced an inconsistent inhibition of the collagen-induced platelet aggregation (1/5 and 2/5 for the respective groups), whereas the response to ADP and thrombin was not altered. Capillary bleeding time was not significantly altered after the ASA administration. Platelet count and screening tests were not influenced by ASA application. According to the results of this study, ASA as a platelet aggregation inhibitor is not useful for the prophylaxis of thromboembolism in cats.

Adenosine Diphosphate↗
PubMed2006

Estradiol increases platelet aggregation in Pl(A1/A1) individuals.

BACKGROUND: The platelet glycoprotein IIb/IIIa receptor is a key mediator of platelet aggregation and intracoronary thrombosis. Studies have suggested that hormone replacement therapy (HRT) may increase coronary events in postmenopausal women. OBJECTIVES: We sought to characterize the relationship between the estrogen concentration expected in HRT and platelet aggregation. DESIGN AND RESULTS: Platelet aggregation studies were performed using epinephrine on 30 healthy individuals (15 Pl(A1/A1) and 15 Pl(A1/A2)) before and after incubation with beta-estradiol (E2) (10(-11) mol/L). The effect of E2 10(-11) mol/L on Pl(A1/A1) platelets demonstrated a significant increase (P = .03) in aggregation compared with baseline. In contrast, with the same concentration of E2, aggregation of Pl(A1/A2) platelets decreased significantly compared with baseline (P < .0001). CONCLUSIONS: Estrogen concentration similar to that expected in HRT resulted in an increase in platelet aggregation in Pl(A1/A1) individuals, but not in Pl(A1/A2) individuals. The data may provide further insight for the increase in coronary events seen in HRT clinical trials and suggest that further evaluation is needed to better define the role of pharmacogenetics in HRT.

Antigens, Neoplasm↗
PubMed1994

Modification of platelet aggregation by leukocytes in acute ischemic stroke.

BACKGROUND AND PURPOSE: Platelet aggregation plays an important role in the pathogenesis of thromboembolic cerebrovascular disease. Leukocytes can efficiently stimulate as well as inhibit platelet aggregability. We studied the influence of leukocytes on collagen-induced platelet aggregation in patients with acute ischemic stroke. METHODS: We investigated 23 patients within 2 days after stroke and 23 healthy age- and sex-matched control subjects and determined collagen-induced platelet aggregation in platelet-rich plasma with or without addition of polymorphonuclear or mononuclear leukocytes. RESULTS: Platelet aggregation without leukocytes tended to be lower in patients than in control subjects (P = .06). Mononuclear leukocytes reduced (P = .018) and polymorphonuclear leukocytes tended to reduce (P = .06) platelet aggregation in patients. Leukocytes did not significantly alter platelet aggregation in control subjects. In the presence of either mononuclear or polymorphonuclear leukocytes, platelet aggregation was significantly lower in patients than in control subjects (P = .004 and P = .008). The ratio of polymorphonuclear leukocytes to platelets in venous blood was higher in patients than in control subjects (P < .001). CONCLUSIONS: Mononuclear--and less clearly polymorphonuclear-leukocytes possess a platelet aggregation-inhibiting potential in the early stages after ischemic stroke, a feature with possible antithrombotic effects.

Acute Disease↗
PubMed2004

Inhibitory effect of GBH on platelet aggregation through inhibition of intracellular Ca2+ mobilization in activated human platelets.

Geiji-Bokryung-Hwan (GBH) was studied on antiplatelet activity in human platelet suspensions. GBH consists of the 5 herbs Cinnamomi Ramulus, Poria Cocos, Mountan Cortex Radicis, Paeoniae Radix, and Persicae Semen, which have been used in herbal medicine for thousands of years for atherosclerosis. The mechanism involved in the antiplatelet activity of GBH in human platelet suspensions was investigated. GBH inhibited platelet aggregation and Ca2+ mobilization in a concentration-dependent manner without increasing intracellular cyclic AMP and cyclic GMP. GBH had no inhibitory effect on thromboxane B2 (TXB2) production in cell-free systems. Collagen-related peptide (CRP)-induced Ca2+ mobilization is regulated by phospholipase C-2 (PLC-gamma2) activation. We evaluated the effect of GBH on tyrosine phosphorylation of PLC-gamma2 and the production of inositol-1,4,5-trisphosphate (IP3). GBH at concentrations that inhibited platelet aggregation and Ca2+ mobilization had no effects on tyrosine phosphorylation of PLC-gamma2 or on the formation of IP3 induced by CRP. Similar results were obtained with thrombin-induced platelet activation. GBH inhibited platelet aggregation and Ca2+ mobilization induced by thrombin without affecting the production of IP3. We then evaluated the effect of GBH on the binding of IP3 to its receptor. GBH at high concentrations partially blocked the binding of IP3 to its receptor. Therefore, the results suggested that GBH suppresses Ca2+ mobilization at a step distal to IP3 formation. GBH may provide a good tool for investigating Ca2+ mobilization.

Blood Platelets↗
PubMed1992

[Development of myocardial infarction in aspirin-treated unstable angina pectoris. Repeated studies of platelet aggregation and of the thromboxane-prostacyclin system].

Platelet functional parameters (platelet aggregation, blood circulating reversibly and irreversibly aggregated platelet complexes, thromboxane B2, 6-keto-PGF1 alpha) were examined in unstable angina treated with aspirin in a daily dose of 320 mg in relation to the outcome of the disease: Group 1, stabilization and Group 2, evolving myocardial infarction. Differences were found in the baseline platelet functional parameters between the groups. The findings suggest that platelet functional parameters show a varying response to aspirin depending on the outcome of the disease. Despite the effective inhibition of thromboxane A2 synthesis, aspirin was found to fail to prevent enhanced platelet aggregatory activity in case of myocardial infarction developed during the therapy.

Adult↗
PubMed1981

Increased circulating platelet aggregates in thalassaemia.

Examination for circulating platelet aggregates according to Wu and Hoak revealed increased circulating platelet aggregates in 71% of splenectomized and 35% of nonsplenectomized patients with beta (0)-thalassaemia/Hb E disease. This may be causally related to the newly observed high incidences of pulmonary artery thrombosis and hypoxaemia in splenectomized thalassaemic patients. It is recommended that anti-platelet aggregation drugs such as aspirin and/or dipyridamole are given to thalassaemic patients after splenectomy.

Humans↗