Increased Platelet Aggregates in Patients With Transient Ischemic Attacks
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In order to evaluate the pathogenetic importance of platelet aggregates in cerebrovascular disease, a platelet count ratio method was used to study 66 patients with transient ischemic attacks (TIAs). Thirty normal subjects and 22 patients without thromboembolic disorders were also included as controls. The mean platelet aggregate ratio of the TIA group was 0.75 ± 0.03 SEM which was significantly lower than that of normal subjects (0.90 ± 0.02) or patient controls (0.88 ± 0.01) (P < 0.01). Seventeen patients with TIA were then treated with aspirin (1,200 mg) and dipyridamole (200 mg) daily. The platelet aggregate ratios were normalized in 13 patients. Of four patients who did not respond to this regimen, one did respond to sulfinpyrazone. When sulfinpyrazone was discontinued, recurrence of symptoms was preceded by an increase in platelet aggregates. These findings suggest that platelet aggregates may play an important role in the pathogenesis of cerebrovascular insufficiency. The determination of platelet aggregates appears useful in selecting patients for antiplatelet therapy.Keywords:
Transient (computer programming)
Stroke
<sup>111</sup>In-labelled human platelets were aggregated with ADP and subjected to ultra-structural morphometric analysis. In addition, the hemostatic function in vivo and the ultra-structural morphology ex vivo of rabbit platelets were examined. The platelet isolation and labelling procedures exerted no certain influence on the aggregation response, and platelet surface/volume calculations did not indicate that platelet activation had taken place. Bleeding time experiments in rabbits indicated that the hemostatic effectiveness of the labelled platelets was unimpaired. Transfused <sup>111</sup>In-labelled platelets isolated from the recipient rabbits exhibited fewer electronmicroscopic signs of platelet activation than the same platelets prior to transfusion. Our results indicate that the described procedure for isolation and <sup>111</sup>In-labelling of platelets induces only insignificant damage to the platelets.
Mean platelet volume
Ex vivo
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Objective Human platelets vary in size, function, and age. Large platelets are often considered to be young platelets. Two situations have to be distinguished, normal steady state platelet production and increased platelet turnover. Here we focused on large and small platelets in humans during increased platelet turnover. To avoid artefacts by interfering factors (medication, comorbidities), we established a platelet apheresis model to deplete platelets from healthy volunteers with subsequent increased platelet production.
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Platelet aggregation was studied at 37 degrees C in citrated whole human blood, using the Ultra Flo 100 Whole Blood Platelet Counter. Aggregation was measured as a fall in the number of single platelets following addition of an aggregating agent. At peak aggregation, the fall in the number of platelets induced by ADP (10 microM), collagen (1 microgram/ml) or thrombin (0.2 U/ml) was about 90%. When blood was incubated with the prostacyclin-analogue ZK36374, the aggregation responses to ADP, collagen and thrombin were reduced with IC50's = 0.5, 1.5 and 3 nM respectively and the corresponding IC100's were: 1, 3 and 12 nM. When ZK36374 was added at peak aggregation, the number of single platelets increased significantly due to disaggregation of preformed platelet aggregates. It is concluded that the present technique represents a rapid, sensitive and more physiological approach for investigating the effects of pharmacological agents on platelet aggregation.
Human blood
Agrégation
Adenosine diphosphate
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SUMMARY. Average platelet size, platelet count, and 35 S‐incorporation into platelets were compared as methods for the measurement of thrombopoietin‐stimulated thrombopoiesis. In mice injected with rabbit anti‐mouse platelet serum (RAMPS) average platelet size was shown to be increased as mice were recovering from thrombocytopenia. Also, 35 S‐measurements on platelets of these mice showed significant increases in cpm/average platelet 2–4 days after RAMPS treatment. Significant increases in 35 S‐incorporation into the total circulating mass of platelets were found on days 3–4. In normal mice or mice in rebound‐thrombocytosis injected with thrombopoietin, platelet size remained unchanged, whereas the platelet count and 35 S‐incorporation into platelets were shown to be significantly increased. Moreover, a dose‐response experiment in mice pretreated with RAMPS showed a slight increase in platelet count as the dose of TSF was increased, but platelet sizes were unaltered. The % 35 S‐incorporation into platelets showed a significant linear dose‐response, i.e. as the dose of thrombopoietin was increased, an increase in % 35 S‐incorporation into platelets was observed. These data indicated that of the three indirect measurements of thrombopoietin, the % 35 S‐incorporation into mouse platelets was the most sensitive, followed by platelet counting; the least sensitive measurement of thrombopoiesis was change in platelet size.
Thrombopoiesis
Mean platelet volume
Thrombocytosis
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Thromboxane B2
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Abstract 51 Cr‐labeled autologous platelets were infused into splenectomized subjects and the specific radioactivities of high‐density (HD) and low‐density (LD) platelet subpopulations were determined sequentially in postinfusion samples. A rapid decrease in the specific radioactivity of LD cohorts (T 1/2 = 2.5 days) was observed, but the specific radioactivity of HD platelets remained constant or increased slightly during the first 4 days and then gradually declined for the next 5 days. No experimental artifacts during the platelet‐labeling steps that could account for these results were demonstrated. These findings confirm previous observations in eusplenic individuals and support the hypothesis that human LD platelets are, on the average, younger than HD platelets. LD platelets contain 33.8 ± 13.5 ng serotonin (5HT)/10 8 platelets and HD platelets 76.8 ± 9.5 ng 5HT/10 8 platelets (P < 0.001). Sequential measurements of 5HT in PRP platelets were performed during the recovery phase of thrombocytopenia following splenectomy in patients with idiopathic thrombocytopenic purpura (ITP), a condition associated with aging of platelets in circulation. Presplenectomy platelet 5HT was 17.7 ng/10 8 platelets and on days 1, 6, and 12 after surgery it increased to 18.1, 37.8, and 61.0 ng/10 8 platelets (n = 7). When three healthy volunteers were given aspirin (500 mg/day) for up to 15 days, no significant change in the 5HT content of circulating platelets was observed. If aspirin blocks, at least partially, the secretory process in vivo without interfering the 5HT uptake by the platelets, this finding stands against the possibility that a net depletion of 5HT occurs during the life‐span of normal human platelets. The observation that human HD platelets, enriched with older cells, contain more 5HT than LD platelets taken together with the parallel increase in platelet 5HT and age during the recovery from thrombocytopenia in ITP patients and the lack of effect of aspirin on platelet 5HT content, provides initial evidence that human platelets accumulate 5HT during their life‐span in circulation.
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The function of 111 In‐labelled platelets has been assessed by collagen‐induced aggregation of platelets in samples of whole blood. The blood samples were drawn after injection of autologous 111 In‐labelled platelets in 19 subjects undergoing platelet kinetic studies. It was thus possible to measure the aggregability of labelled and unmanipulated platelets simultaneously. 111 In‐labelled platelets aggregated to the same extent as unmanipulated platelets when tested from 10 min to 24 h after injection of the labelled platelets. The results confirm the assumption that minimal damage is inflicted on the platelets during the isolation and labelling procedures, and support the concept that platelets manipulated in vitro may recover in vivo within a few minutes after reinjection.
Ex vivo
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Thromboxane B2
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Adenine nucleotide
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In the previous communication, suggestive evidence was presented for large-heavy platelets being "young" platelets and light-small platelets being "old" platelets. Large-heavy, light-small, and total human platelet populations were compared with respect to their platelet function. After addition of adenosine diphosphate (ADP), thrombin, or epinephrine, platelet aggregation time was 3.0-, 4.5-, and 3.3-fold shorter with large-heavy platelets compared with light-small platelets, and large-heavy platelets released 3.7-, 7.6-, and 8.1-fold greater adenosine triphosphate (ATP) into the medium, respectively, than did light-small platelets. After platelet aggregation by thrombin or epinephrine, large-heavy platelets released 6.0- and 3.8-fold more ADP into the medium than did light-small platelets. After platelet aggregation by ADP, light-small platelets consumed 5.9-fold greater added extracellular ADP than did large-heavy platelets.Large-heavy platelets aggregated by ADP, thrombin, or epinephrine released 9.1-, 8.5-, and 12.7-fold greater platelet factor 4 than light-small platelets similarly treated.
Adenosine diphosphate
Adenine nucleotide
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