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At least 19 recordsLinked to original sources
PubMed1975

[Measurement of spontaneous platelet aggregation. Platelet aggregation test III (author's transl)].

A new measuring device for the estimation of the "spontaneous" aggregating activity of thrombocytes has been developed. In this photometric platelet aggregation test (PAT III) a small amount (0.6 ml) of platelet-rich plasma (PRP) is being rotated in a disc-shaped cuvette at 20 rpm, at 37% C. Changes in optical density of PRP which are induced by the formation of platelet aggregates are continuously registered using a chart recorder. The decisive trigger mechanism for aggregation is an increase of plasma pH in the rotating sample which is caused by evaporation of CO2. The results of the test depend on the platelet count in PRP. Aggregation curves are misrepresented by admixture of erythrocytes and lipid turbidity. The tendency of platelets to aggregate increases within 60-90 min following blood sampling. During this period the time interval to the onset of aggregation(Tr) is shortening, and the maximum aggregation speed (alpha2) is increasing. The spontaneously enhanced aggregation tendency of thrombocytes may be reliably measured from 60 min after drawing the blood. The reason for these time-dependent changes which are also demonstrable in ADP-collagen-or epinephrine-induced aggregation is probably the primary shape change of platelets, which occurs after blood drawing and makes them "stickly" and aggregable. PAT III was developed for the detection of enhanced platelet aggregation, indicating a risk of thrombosis and thromboembolic omplications. The new measuring device has been designed as "universal" aggregometer. Additional equipment is available for the registration of ADP-collagen-or epinephrine-induced aggregation similar to Born's and O'Brien's methods. The device may be mounted easily on an Eppendorf photometer without further modifications.

Adenosine Diphosphate↗
PubMed1976

On the measurement of spontaneous platelet aggregation. The platelet aggregation test III. Methods and first clinical results.

A new measuring device was developed for the study of "spontaneous" aggregating activity of thrombocytes. In the photometric platelet aggregation test (PAT III) 0.6 ml of platelet-rich plasma (PRP) are rotated in a disc-shaped cuvette at 20 rpm and 37 degrees C. Changes in optical density of PRP which are induced by the formation of platelet aggregates are continuously registered using a chart recorder. PAT III was developed for the detection of enhanced platelet aggregation, indicating a risk of thrombosis and thromboembolic complications. In 146 healthy individuals a certain percentage showed slight primary aggregation (alpha1) which in some cases was followed by marked aggregation (alpha2) at a certain time (Tr) after the beginning of rotation. The percentage of individuals showing alpha2 increased with age. An increase of plasma pH in the rotating sample, which was caused by diffusion of CO2, was an important conditioning factor for aggregation. The test results depended on the platelet count in PRP. Aggregation curves were suppressed by admixture of erythrocytes and lipid turbidity. The tendency of platelets to aggregate increased within 60-90 min following blood sampling. During this period the interval to the onset of aggregation (Tr) became shorter and the maximum aggregation speed (alpha 2) increased with time. PAT III yielded reproducible results when it was carried out more than 60 min after blood drawing. In a group of 327 diabetic patients "spontaneous" aggregation occurred more frequently in all age groups as compared with the controls. Additional equipment was available for the registration of ADP-, collagen-, or epinephrine-induced aggregation similar to Born's and O'Brien's method. The device can easily be mounted on an Eppendorf photometer without further alterations.

Age Factors↗
PubMed1992

Circulating aggregated platelets, number of platelets per aggregate, and platelet size during acute myocardial infarction.

Circulating aggregated platelets (total, reversibly and irreversibly aggregated), the number of platelets per aggregate and "big" platelets were measured by a modification of the Wu and Hoak method in 42 patients on the first, second and fifth day of acute myocardial infarction (AMI). Among them, 30 had an uncomplicated course and 12 patients had complications that occurred between the 5th and 10th day of hospitalization (7 patients had reinfarction and 5 died). In all patients the measured parameters were elevated compared with those of control subjects. There was a significant increase, especially after the first observation day, in the values of total aggregated platelets (37 +/- 11% vs 26 +/- 12%, p < 0.001), reversibly aggregated platelets (27 +/- 9% vs 17 +/- 8%, p < 0.001) and the average platelets per aggregate (8.6 +/- 0.3 vs. 2.3 +/- 0.4) in patients with versus without complications. In considering the role of platelets in the development of AMI, these findings may add information to the role of platelets in determining the course of AMI.

Blood Platelets↗
PubMed1976

The effect of vitamin E on platelet aggregation.

Platelet aggregation studies were performed in five men with coronary artery disease and angina pectoris and five men with nonspecific chest pain before and after receiving 1,000 I.U. of alpha-tocopherol acetate orally per day for 8 days. There was no significant difference in the platelet aggregation response to three concentrations of ADP and two concentrations of epinephrine between the pre- and post-vitamin E periods among the 10 patients. If tocopherol acetate (vitamin E) has any beneficial effect on the prevention of thromboemolism or in the treatment of angina pectoris and peripheral vascular disease, it is not via inhibition of platelet aggregation.

Adenosine Diphosphate↗
PubMed1977

Autoprothrombin ii-a, thrombin, and epinephrine: interrelated effects on platelet aggregation.

Platelets aggregate with thrombin-free autoprothrombin II-A. Aggregation was dependent on an intact release mechanism since inhibition of aggregation occurred with adenosine, colchicine, or EDTA. Autoprothrombin II-A reduced the sensitivity of platelets to aggregate with thrombin, but enhanced epinephrine-mediated aggregation. Autoprothrombin II-A directly competes for membrane sites sensitive to thrombin. It allows complexes to from with epinephrine. There was no absolute requirement for autoprothrombin II-A since epinephrine aggregated dog platelets at the identical optimum concentration following Coumadin treatment.

Animals↗
PubMed1976

The effect of cytosine arabinoside on platelet aggregation.

Platelet aggregation induced by ADP, collagen, epinephrine, and thrombin was studied in patients with acute leukemia in complete remission, before and after a continuous 5-day intravenous infusion of cytosine arabinoside at a dose of 100 mg/m2 per day. Aggregation was also measured in normal subjects with cytosine arabinoside added in vitro. Cytosine arabinoside had no significant effect on platelet aggregation after either in vitro or in vivo administration.

Acute Disease↗
PubMed1976

The effect of thrombocytopenia on the determination of platelet aggregation.

Platelet aggregation has been widely assumed to be unmeasurable in thrombocytopenic samples. Using a sensitive differential self differential self-calibrating aggregometer, and standard aggregating agents, aggregation was measured in serially diluted platelet-rich plasma. Aggregation induced by ADP or collagen was reproducible at platelet counts as low as 50,000 per cu. mm., and with epinephrine aggregation was reproducible at platelet counts as low as 75,000 per cu. mm.

Adenosine Diphosphate↗
PubMed1977

Androgen-mediated sensitivity in platelet aggregation.

Platelet responsiveness to an aggregating stimulus (ADP) was greater (X10) in male than in female rats. Castration reduced aggregability in males (X4) and increased it in females (X3). Pretreatment with testosterone (1 mg/kg, sc) enhanced platelet aggregability in both sexes and restored the diminished responsivity observed in castrated males. Incubation of platelets with testosterone (1-10 ng/ml) potentiated rat (18.0 +/- 1.5%) and guinea pig (40.0 +/- 5.0%) aggregability when compared with vehicle-treated platelets. Estradiol (1 mg/kg, sc) in vivo or estradiol, progesterone, and deoxycorticosterone (1 microng/ml) in vitro had the opposite effect and decreased aggregability. The rank order of effectiveness of androgens in vitro was dihydrotestosterone, testosterone, methyltestosterone, androstendione, and androsterone, which correlates with their androgenicity. The effect of androgens was antagonized in vitro by the antiandrogen (Flutamide) and by estradiol. These data suggest that gonadal steroids may play a role in regulating platelet function in the rat and guinea pig.

Adenosine Diphosphate↗
PubMed1977

Marathon run II: Effects on platelet aggregation.

Platelet count and aggregation were assessed in 9 Finnish amateur runners aged 34 to 48, and one 65-year old taking part in a non-competitive marathon race (42.2 km). After the run the mean value of platelet count showed a very significant rise (p less than 0.001). The platelets were markedly more sensitive to both ADP and collagen-induced aggregation. A highly significant increase (p less than 0.001) was noted for both the intensity and velocity of platelet aggregation. The finding of platelet by hyperaggregability after prolonged strenous exercise even in trained subjects is discussed. It is concluded that a through medical examination of the haemostatic balance is recommended before a marathon race.

Adenosine Diphosphate↗
PubMed1978

Platelet monoamine oxidase and epinephrine-induced platelet aggregation.

Platelet MAO activity and the aggregation response to epinephrine, ADP, and collagen were measured in normal subjects. There was a direct correlation between the amount of platelet MAO activity and the per cent aggregation induced by 1 and 2 micrometer epinephrine. There were lesser correlations between platelet MAO and ADP or collagen-induced aggregation. These findings suggest that platelet MAO may play a role in determining the response of human platelets to epinephrine.

Adenosine Diphosphate↗
PubMed1979

Release of platelet fibronectin (cold-insoluble globulin) from alpha granules induced by thrombin or collagen; lack of requirement for plasma fibronectin in ADP-induced platelet aggregation.

Platelets lysed with Triton X-100 contain 3.44 +/- 1.27 (SD) microgram of fibronectin (cold-insoluble globulin) per 10(9) platelets. Fibronectin was partially released from washed whole platelets by collagen or thrombin, and its release by collagen was inhibited by aspirin. Analysis of subcellular fractions obtained by density-gradient centrifugation of disrupted platelets indicated that fibronectin was contained in the alpha granules. Fibrinogen depleted of fibronectin (less than 2 microgram/mg) supported ADP-induced aggregation as effectively as fibrinogen contaminated with this protein, thus reinforcing the generally held view that fibrinogen itself is the necessary protein cofactor in this reaction.

Adenosine Diphosphate↗
PubMed1991

The inhibition of platelet aggregation of metastatic H-ras-transformed 10T1/2 fibroblasts with castanospermine, an N-linked glycoprotein processing inhibitor.

A series of T24-H-ras-transformed 10T1/2 fibroblasts with varying metastatic potential was tested for the ability to aggregate platelets. Results indicate that although platelet activation was always detected in the highly metastatic cells, some non-metastatic cells also have the ability to cause platelet aggregation, suggesting that this is a necessary but not sufficient characteristic of the metastatic phenotype. Apyrase, an ADP scavenger, effectively inhibited platelet aggregation by metastatic cells, however, there was no significant increase in ADP secretion or relation to the ability of the tumor cells to activate platelets. Hirudin, a thrombin inhibitor, did not affect aggregation, suggesting that the pathway of activation is thrombin-independent. The glycoprotein processing inhibitor, castanospermine, which reduces glycosidase I activity and metastatic capability, inhibited the ability of metastatic cells to cause platelet aggregation. However, another inhibitor of oligosaccharide processing, swainsonine, which inhibits mannosidase II activity and does not reduce metastasis, had no effect on platelet aggregation. These results show that the integrity of N-linked oligosaccharide structure of glycoproteins is an important feature of the ability of ras-transformed fibroblasts to activate platelets.

Adenosine Diphosphate↗
PubMed1990

Iloprost and tissue-type plasminogen activator differentially affect platelet aggregation in platelet-rich plasma and in whole blood.

Platelet aggregation in platelet-rich plasma (PRP) is more sensitive to agonists and more resistant to antagonists than that in whole blood. In this study, we show that the presence of neutrophils in whole blood accounts at least in part for diminished platelet aggregation in whole blood. The platelet-inhibitory effect of neutrophils relates to the release of nitric oxide and not to elastase or adenosine. Furthermore, two unrelated platelet inhibitors, iloprost and tissue-type plasminogen inhibitor, decrease platelet aggregation to a greater extent in whole blood than in PRP. However, these agents exert cumulative or synergistic inhibitory effects with neutrophils on platelet aggregation in PRP. Thus, the inhibition of platelet aggregation in vivo may relate to the interaction between neutrophils and platelet-inhibitory agents.

Blood Physiological Phenomena↗
PubMed1991

Human colorectal adenocarcinoma cells: differential nitric oxide synthesis determines their ability to aggregate platelets.

The existence and role of an L-arginine:nitric oxide (NO) pathway in two human colorectal adenocarcinoma cell lines, SW-480 and SW-620, were investigated. Both cell lines, which derive from the same patient, SW-480 from the primary tumor and SW-620 from its metastatic lesion, were shown to have a cytosolic, Ca(2+)-independent, NADPH-dependent NO synthase, the activity of which was lower in the cytosol of SW-620. These cells were more potent inducers of platelet aggregation. In contrast, SW-480, which had more NO synthase activity, were less potent inducers of platelet aggregation. Pretreatment of both cell lines with NG-monomethyl-L-arginine, an inhibitor of NO synthase, potentiated their proaggregating effect and made them equally active. Exogenous L-arginine, NO, and related nitrovasodilators all inhibited platelet aggregation induced by SW-620. The antiaggregating activity of NO was further potentiated by prostacyclin and by M&B22948, a selective inhibitor of cyclic GMP phosphodiesterase. We propose that the generation of NO by tumor cells inversely correlates with their metastatic potential. Furthermore, we show that the lower activity of NO synthase in metastatic cells is due to the presence in these cells of a low molecular weight inhibitor of the NO synthase. In addition, agents which modulate platelet function by a cyclic GMP-dependent mechanism may be useful in the prevention of tumor metastasis.

Adenocarcinoma↗
PubMed1976

Factor VIII and human platelet aggregation. I. Evience that the platelet aggregating activity of bovine factor VIII is a property of its 'carrier protein' subunit.

Bovine factor VIII is a potent inducer of aggregation of human platelets. Upon gel filtration of five-thousand-fold purified material in 0.5 M CaCl2, bovine factor VIII is separated into high and low molecular weight components; the former contains both a 'carrier protein' and platelet aggregating activity, the latter the procoagulant activity (low molecular weight factor VII, LMW-FVIII). Upon removal of Ca2+ ions, LMW-F VIII recombines with the 'carrier protein'. LMW-F VIII modifies aggregation by 'carrier protein', but not aggregation by undissociated bovine factor VII, adenosine-5'-diphosphate or adrenaline. This finding indicates that the platelet aggregating activity in indeed a property of the 'carrier protein'.

Animals↗