[Effects of 2 doses of lysine acetylsalicylate on platelet aggregation, beta-thromboglobulin and platelet factor 4 in aged atherosclerotic patients].
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Aged↗
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[Effect of raubasine and pipratecol on platelet aggregation and on the platelet release reaction].
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Adenine Nucleotides↗
The filter loop technique as a method of measuring platelet aggregation in the flowing blood of the rat; the inhibitory activity of 5-oxo-1-cyclopentene-1-heptanoic acid (AY-16,804) on platelet aggregation.
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Adenosine Diphosphate↗
Characterization of the normal bovine platelet aggregation response.
1. Bovine platelets are more sensitive to stimulation by platelet activating factor (PAF) than adenosine-di-phosphate (ADP) or thrombin. 2. While epinephrine, arachidonic acid and serotonin are ineffective by themselves as aggregatory stimulants of bovine platelets they enhance the aggregation response of other platelet agonists. 3. There is no correlation between thromboxane A2 production and release and the extent of platelet aggregation in bovine platelets. 4. The dependence of bovine platelet aggregation on a phospholipid pathway and calcium mobilization is indicated.
Adenosine Diphosphate↗
Tumor cell-platelet aggregation: induced by cathepsin B-like proteinase and inhibited by prostacyclin.
The ability of tumor cells to metastasize may be related to their ability to promote aggregation of host platelets. The use of inhibitors of cysteine proteinases resulted in parallel inhibition of B16 amelanotic melanoma-induced platelet aggregation and of a cathepsin B activity. The antimetastatic agent prostacyclin inhibited platelet aggregation induced by the tumor cells and by papain, a cathepsin B-mimicking agent.
Animals↗
[Comparison of platelet activators used in slide platelet aggregation test].
The study was purposed to explore the suitable platelet activators to be used in slide platelet aggregation test. Experiments were as follows: (1) to detect the intensity and time in 15 healthy donors' platelet aggregation tests induced by cationic propyl gallate (c-PG) and the usual platelet activators: ADP, collagen, epinephrine, arachidonic acid and ristocentin, respectively; (2) to detect the time in platelet aggregation tests of 15 healthy donors induced by c-PG and the above usual platelet activators respectively after addition of PGI2, cAMP or EDTA; (3) to detect the time in 15 healthy donors' platelet aggregation tests induced by c-PG after addition of heparin; (4) to detect the intensity and time of platelet aggregation induced by c-PG at the platelet count of (240-15) x 10(9)/L, (5) to detect the time of platelet aggregation induced by c-PG in eight patients each of whom had taken 100 mg aspirin per day for five days. The results showed that (1) c-PG reduced the strongest intensity of platelet aggregation and the time taken was appropriate, (2) c-PG was the most effective activator to reveal the inhibitive effect on platelet by PGI2, cAMP or EDTA, (3) 0.5 - 3 U/ml heparin did not significantly change the platelet aggregation induced by c-PG, (4) 15 healthy donors' platelet aggregation induced by c-PG displayed clearly on the slide until the platelet count below 30 x 10(9)/L, (5) The platelet aggregation time induced by c-PG was significantly prolonged in eight patients who had taken aspirin. In conclusion, compared to the usual platelet activators, c-PG has remarkable potential advantages when used in slide platelet aggregation test.
Cyclic AMP↗
The role of platelet aggregation and release in fragment D-induced pulmonary dysfunction.
The plasma concentration of fibrinogen degradation product D (fragmentt D) is markedly incrased following major burn or traumatic injury. Purified human fragment D infused into awake, restrained, nontraumatized rabbits (100 micrograms/ml blood) causes progressive thrombocytopenia, pulmonary dysfunction, vascular leak, and interstitial neutrophilia. Rabbits treated with the antihistamine diphenhydramine (Benadryl) prior to fragment D infusion fail to develop these symptoms. This study examined platelet aggregation, platelet ATP secretion, and platelet malondialdehyde release in rabbits which received fragmen D alone or fragment D following diphenhydramine pretreatment. Platelet-rich plasma was prepared from citrated blood drawn from femoral arterial catheters at 0, 2 1/2, and 4 hours postinfusion. Platelet aggregation was stimulated with either collagen or ADP. Malondialdehyde, a byproduct of thromboxane synthesis, was measured by colorimetry. Platelet aggregation and function (stimulated with collagen) were enhanced in fragment D platelet-rich plasma, since all response times decreased. Total ATP and MDA release incresed. Diphenhydramine pretreatment inhibited fragment D-enhanced aggregation, ATP release and prostaglandin (thromboxane) synthesis. No animal pretreated with diphenhydramine exhibited thrombocytopenia or respiratory dysfunction. Stimulation of platelet aggregation and release may represent one mechanism by which fragment D induces pulmonary dysfunction. Diphenhydramine inhibits these responses and may prove therapeutic in posttraumtic pulmonary complications.
Adenosine Diphosphate↗
Adrenaline and adenosine diphosphate-induced platelet aggregation require shape change. Importance of pseudopods.
The requirement of platelet shape change for early platelet aggregation measured from the disappearance of singlet platelets is compared for ADP and adrenaline. Platelet shape change is measured from pseudopod formation or from a change in main body volume or axial ratio. In the absence of shape change, platelets have a smooth discoid form and are referred to as discocytes. Citrated platelet-rich plasma prepared at 37 degrees C contains approximately 65% discocytes and approximately 35% discoid platelets, which possess pseudopods. The addition of ADP causes all platelets to change shape (pseudopods axial ratio and body volume) and 80% to 90% platelet aggregation. On the other hand, adrenaline causes only an approximately 15% increase in shape-changed platelets (pseudopods only) and approximately 33% platelet aggregation, in the presence of apyrase to minimize the effects of released ADP. Measurements of the shape of the nonaggregated platelets in the presence and absence of ongoing platelet aggregation induced by either ADP or adrenaline indicate that discocytes are not recruited into aggregates. For both ADP and adrenaline, the extent of platelet aggregation exceeds the extent of platelet shape change as measured from the disappearance of discocytes. However, in both cases, platelet aggregation does not exceed the total number of shape-changed platelets (i.e., pseudopods plus newly shape-changed discocytes), indicating that the pseudopods are also participating in platelet aggregation. Our results suggest that pseudopod formation is a common requirement for ADP- and adrenaline-induced platelet aggregation and is of greater importance than either changes in main body volume or axial ratio.
Adenosine Diphosphate↗
Alteration of platelet aggregation by cigarette smoke and carbon monoxide.
Platelet aggregation with epinephrine, adenosine diphosphate and arachidonic acid was studied in the presence of cigarette smoke and carbon monoxide. It is shown that cigarette smoke inhibits the arachidonic acid induced platelet aggregation as well as the second phase of epinephrine induced aggregation. The adenosine diphosphate induced platelet aggregation is not significantly affected by cigarette smoke. Carbon monoxide causes similar alterations in platelet aggregation. These results suggest that cigarette smoke inhibits platelet aggregation. This aggregation inhibition is due to the presence of carbon monoxide.
Carbon Monoxide↗
Tumour-cell-induced platelet aggregation: studies with cloned metastatic and non-metastatic variants.
Blood platelets have been suggested to play an important role in modulating the development of experimental metastases. Tumour cells can induce platelet aggregation in vitro and a number of mechanisms have been proposed to explain the in vivo and in vitro observations. In the present study, we used tumour cells cloned from B16 melanoma and mouse mammary tumour virus (MMTV) carcinoma polyclonal populations to check whether tumour cells with low- and high-metastatic behaviour in vivo had different quantitative and qualitative platelet-aggregating activity in vitro. We found no significant quantitative difference between platelet aggregation induced by the low- and the high-metastatic clones. Indeed both the high and the low metastatic B16 melanoma clones poorly aggregated platelets, while both the high and low metastatic MMTV carcinoma clones efficiently aggregated platelets. Both the B16 melanoma and the MMTV carcinoma parental cell lines, which can be classed as intermediate metastatic, aggregated platelets well. However, based on the results with heparin and creatine phosphate/creatine phosphokinase, it appeared that qualitative differences might exist in the mechanism of platelet aggregation by tumour cells. For the parental lines and highly metastatic clone C1 a thrombin-linked component was more important than an ADP-like component, which was nevertheless present, to promote platelet aggregation. For the low-metastatic clone C2, the ADP-like component appeared to be the most important.
Adenosine Diphosphate↗
Quantitative detection of platelet aggregates in whole blood without fixation.
Platelet counting detects lesser degrees of platelet aggregation than conventional aggregometry. In order to prevent progressive platelet aggregation or disaggregation after sampling it is customary to fix blood samples. However fixation may introduce other artefacts. We first compared stability of platelet counts in EDTA-, citrate- and r-hirudin-anticoagulated blood from healthy volunteers. Second, the stability of platelet counts in unfixed EDTA- and hirudin-anticoagulated blood was compared with glutaraldehyde-fixed blood in the same anticoagulants. Third, the effect of in vivo heparin administration on platelet counts in EDTA- and hirudin-anticoagulated blood was studied. Platelet counts within 2 h of collection were significantly higher in EDTA- than in hirudin- or citrate-anticoagulated blood (P = 0.002 vs. hirudin and P = 0.001 vs. citrate). Twenty-four hour counts in hirudin and EDTA were unchanged (P = 0.3 and P = 0.2, respectively, vs. earlier counts). Counts in citrate increased significantly (P = 0.007; n = 10). Platelet counts in fixed blood did not differ significantly from those in unfixed blood. Heparin administered for cardiopulmonary bypass reduced platelet counts in hirudin-anticoagulated blood from (mean +/- 1 standard deviation) 180 +/- 45 to 162 +/- 30 x 10(9) l-1 (P = 0.01; n = 14), without significantly lowering counts with EDTA-anticoagulation, consistent with increased platelet aggregation. Hirudin and EDTA provided stable platelet counts, suggesting that fixation is unnecessary.
Adult↗
Nonpeptide glycoprotein IIb/IIIa inhibitors. 15. Antithrombotic efficacy of L-738,167, a long-acting GPIIb/IIIa antagonist, correlates with inhibition of adenosine diphosphate-induced platelet aggregation but not with bleeding time prolongation.
The nonpeptide platelet glycoprotein IIb/IIIa antagonist, L-738, 167, was characterized in dog and nonhuman primate. In an anesthetized canine model of coronary artery electrolytic lesion, L-738,167 elicited dose-dependent (3, 4, 4.5 and 5 micrograms/kg i.v.) decreases in incidence of occlusion, reductions in thrombus mass and elevations in bleeding time. Antithrombotic efficacy correlated with inhibition of adenosine diphosphate-induced platelet aggregation but was dissociated from marked bleeding time elevation. Similarly, suppression of platelet-dependent cyclic flow reductions with L-738,167 in the canine coronary artery (5 micrograms/kg i.v.) and African green monkey carotid artery (10 micrograms/kg i.v.) correlated with inhibition of adenosine diphosphate-induced platelet aggregation but not with inhibition of thrombin-induced platelet aggregation or significant prolongation of bleeding time. In conscious dogs and sedated chimpanzees, single dose intravenous bolus (5-20 micrograms/kg) and oral (25-200 micrograms/kg) administration of L-738,167 exhibited long duration (> or = 8 hr) inhibition of ex vivo platelet aggregation. Once daily oral administration to conscious dogs (10-30 micrograms/kg/day for 15 days) and rhesus monkeys (200-250 micrograms/kg/day for 11 days) maintained significant but submaximal (50-90% inhibition) trough levels of inhibition of adenosine diphosphate-induced ex vivo platelet aggregation. Platelet sensitivity to adenosine diphosphate after multiple days of oral dosing in dogs was similar to pretreatment sensitivity. L-738,167 showed characteristics suitable for chronic oral therapy with a glycoprotein IIb/IIIa inhibitor.
Adenosine Diphosphate↗
In vivo platelet aggregation in acute malaria.
Thirteen patients suffering from acute malaria attack and thirteen apparently healthy human volunteers (control) were used for the study. Platelet aggregation was determined by platelet count ratio technique in which a reduction in platelet count ratio signified an increase in platelet aggregation. Platelet count ratio in acute malaria patients was 0.75 +/- 0.03 (SEM). Platelet count ratio in subjects used as control was 0.88 +/- 0.02. This value was significantly higher than the former (P less than 0.001). Platelet count ratio correlated negatively with the degree of parasitaemia (r = -0.71; P less than 0.01). ADP, a platelet aggregating drug, also reduced platelet count ratio in rats significantly. Acute malaria attack therefore enhances platelet aggregation in vivo.
Acute Disease↗
A revised model of platelet aggregation.
In this study we have examined the mechanism of platelet aggregation under physiological flow conditions using an in vitro flow-based platelet aggregation assay and an in vivo rat thrombosis model. Our studies demonstrate an unexpected complexity to the platelet aggregation process in which platelets in flowing blood continuously tether, translocate, and/or detach from the luminal surface of a growing platelet thrombus at both arterial and venous shear rates. Studies of platelets congenitally deficient in von Willebrand factor (vWf) or integrin alpha(IIb)beta(3) demonstrated a key role for platelet vWf in mediating platelet tethering and translocation, whereas integrin alpha(IIb)beta(3) mediated cell arrest. Platelet aggregation under flow appears to be a multistep process involving: (a) exposure of vWf on the surface of immobilized platelets; (b) a reversible phase of platelet aggregation mediated by the binding of GPIbalpha on the surface of free-flowing platelets to vWf on the surface of immobilized platelets; and (c) an irreversible phase of aggregation dependent on integrin alpha(IIb)beta(3). Studies of platelet thrombus formation in vivo demonstrate that this multistep adhesion mechanism is indispensable for platelet aggregation in arterioles and also appears to promote platelet aggregate formation in venules. Together, our studies demonstrate an important role for platelet vWf in initiating the platelet aggregation process under flow and challenge the currently accepted view that the vWf-GPIbalpha interaction is exclusively involved in initiating platelet aggregation at elevated shear rates.
Animals↗
Further studies on the role of red blood cells in spontaneous platelet aggregation.
The influence of red blood cells on platelet aggregation has recently been a subject of considerable interest. We have studied the effect of red cells on spontaneously formed platelet aggregates in rotating vials at 37 degrees C. Platelet aggregation was quantified by measuring the fall in number of single platelets with a whole blood platelet counter. Autologous packed red cells, platelet rich plasma and platelet free plasma were used to reconstitute aliquots of blood with constant platelet count but 0-60% haematocrit (Hct). The fall in platelet count was minimal at zero Hct, increased markedly with the Hct in the anaemic range and less markedly in the normal to polycythaemic ranges of Hct. Scanning electron microscopic observation of whole blood showed the presence of small platelet aggregates after about 3 mins rotation and very large aggregates after about 12 mins. ADP from red cells has been implicated in triggering platelet aggregation in whole blood. Whether aggregates are formed as a result of ADP leaking from the red cells or by their jostling physical action on the platelets is discussed. The marked effect of the red cells on spontaneous platelet aggregation however, justifies the manipulation of the Hct as a useful therapeutic option in the control of thrombotic and bleeding tendencies.
Adult↗
The fibrinogen-dependent pathway of platelet aggregation.
Fibrinogen participates in platelet aggregation induced by ADP and this participation is receptor mediated. The role of fibrinogen in platelet function is not restricted to the ADP stimulus as the molecule may regulate aggregation induced by the direct interaction of the protein with a single, specific receptor system. Thus, a common fibrinogen-dependent mechanism leading to platelet aggregation is hypothesized.
Adenosine Diphosphate↗
Factors influencing platelet aggregation in whole blood.
In order to evaluate the interference of blood cells on platelet aggregation, spontaneous platelet aggregation (SPA), ADP, and collagen-induced platelet aggregation were investigated in whole blood by the impedance method and in platelet-rich plasma (PRP) by densitometric and impedance aggregometers. Stirring of the sample induced a significant decrease of neutrophils (P less than 0.001) but no changes of red blood cell (RBC) and platelet count. After collagen addition, a further decrease of neutrophils was observed, while RBC count was unmodified. The occurrence of SPA was not different in whole blood and in PRP. Platelet number and hematocrit did not affect either spontaneous or collagen-induced aggregation. A significant linear relation (r = -0.60, P less than 0.01) between neutrophil count and collagen whole blood platelet aggregation was found. Collagen- and ADP-induced aggregation were significantly higher and lower, respectively, in whole blood than in PRP using the densitometric method. No differences were observed in SPA and collagen platelet aggregation according to age and sex.
Adult↗
Monitoring modulators of platelet aggregation in a microtiter plate assay.
Platelets play a central role in maintaining biological hemostasis. Inappropriate platelet activation is responsible for thrombotic diseases such as myocardial infarction and stroke. Therefore, novel agents that can inhibit platelet activation are necessary. However, assays that monitor platelet aggregation are generally time-consuming and require high volumes of blood and specialized equipment. Therefore, a medium- to high-throughput assay that can monitor platelet aggregation would be considered useful. Such an assay should be sensitive, comparable to the "gold standard" assay of platelet aggregometry, and able to monitor multiple samples simultaneously but with low assay volumes. We have developed such a microtiter assay. It can assay an average of 60 independent treatments per 60 ml blood donation and demonstrates greater sensitivity than the current gold standard assay, namely platelet aggregation in stirring conditions in a platelet aggregometer. The microtiter plate (MTP) assay can detect known inhibitors of platelet function such as indomethacin, aspirin, and ReoPro. It is highly reproducible when using standard doses of agonists such as thrombin receptor-activating peptide (20 microM) and collagen (0.19 mg/ml). Finally, the MTP assay is rapid and sensitive and can detect unknown platelet-modulating agents from a library of compounds.
Amino Acid Sequence↗