[Platelet function tests (aggregation, release reaction, adhesion)].
Explore the source record for details and available documents.
SEARCH · Search PubMed
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.
Explore the source record for details and available documents.
In 20 patients with peripheral vascular disease treated with prostacyclin (5 ng/kg/min) we observed a significant activation of platelet function as measured by platelet proteins, ADP-induced aggregation platelet sensitivity and platelet count. Only the platelet survival was significantly prolonged by the treatment.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Low-molecular weight dextran sulfate (DXS 5000, M(r) 5 kDa) was found to control selectively complement activation without affecting contact activation. However, DXS 5000 being a glycosaminoglycan (GAG) may inhibit coagulation, which might bear the risk of bleeding complications and limit its clinical use. We investigated the influence of DXS 5000 on the prothrombin time (PT), the activated partial thromboplastin time (aPTT), the thrombin time (TT), the inhibitory capacity of human plasma against activated factor X (FXa), and on platelet function as assessed by the platelet function analyzer (PFA-100) and by platelet aggregation studies. The PT steadily increased with increasing DXS 5000 concentration, whereas the aPTT was already prolonged (>300 s) at low DXS 5000 concentrations (100 microg/ml). The TT was >120 s at DXS 5000 concentrations of 1000 microg/ml. The inhibitory capacity of human plasma against FXa was dose-dependently increased by DXS 5000. With increasing DXS 5000 concentrations, a prolonged PFA-100 closure time (CT) was observed. Detailed aggregation studies revealed a dose-dependent inhibition of platelet aggregation with ristocetin by DXS 5000, whereas aggregation with ADP, collagen, and arachidonate was unaffected. DXS 5000 induces a disturbance of primary and secondary hemostasis.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Routine blood analysis, platelet counts, number of circulating platelet aggregates (CPA) and platelet aggregation in vitro against adenosine-diphosphate (ADP), epinephrine and collagene were studied in 45 healthy controls, in 10 hospitalized patients with other neurological diseases than stroke and in 12 patients with transient ischemic attacks (TIA) before and after prophylactive treatment with anticoagulants (AC) or antiplatelet drugs (APD). Except for lower hemoglobin and hematocrit levels in women, sex, smoking, oral contraceptives of pregnancy did not significantly influence the routine blood parameter. Smoking females taking oral contraceptive had an increased number of CPA and the most easily induced aggregation in vitro. Patients with TIA had no significant differences in blood or platelet findings versus the healthy controls (except smoking females on oral contraceptives) or the non-stroke patients, even though individual patients could have high numbers of CPA and an easily induced platelet aggregation in vitro. Treatment with AC did not influence platelet function, whereas APD therapy decreased the number of CPA and inhibited the secondary platelet aggregation in vitro.
The PFA-100(R) (PFA) diagnostic system for the detection of platelet dysfunction was evaluated to determine reference ranges in a normal population. The PFA determines the primary haemostasis capacity (PHC) of anticoagulated whole blood, expressed by the system's closure time (CT). In this study the CT reference ranges were determined for blood samples collected in 105 mmol/l (3.2%) buffered citrate and the effect of gender, smoking, and use of oral contraceptives on reference ranges was assessed. Each of the 309 healthy blood donors from five blood centres was confirmed to have normal platelet function before inclusion in the study. Blood samples were tested in duplicate with both the collagen/epinephrine (Col/Epi) and collagen/ADP (Col/ADP) test cartridges. PFA reference ranges (90% central intervals of measured closure times) for both cartridge types were similar for all groups. Subgroup analysis showed that neither gender nor oral contraceptive usage had any effect on PHC. The 95% cut-off value for the Col/Epi CT was slightly higher for smokers than for non-smokers, an effect more pronounced in female than in male donors. However, the small difference did not justify establishment of specific reference ranges for smokers. Data from all included subjects were pooled to calculate the CT reference ranges for blood samples collected in 105 mmol/l buffered citrate (Col/Epi 82-150 s; Col/ADP 62-100 s). Normal levels of fibrinogen, as well as normal platelet counts and normal haematocrit levels, appeared not to influence the PHC. Because slight but significant differences of the reference ranges were observed between some of the participating sites, in-house confirmation of these reference range guidelines is recommended.
With a selected spectrum of coagulation tests the functioning capacity of thrombocytes was investigated in rabbits exposed to a whole body irradiation by means of 60Co radiation with a LD 5/30. A reduced retraction could be proved for times of irradiation (the 5th, 8th, 11th, 21st, 35th, and 56th day). A reduced formation of malondialdehyde could be identified in thrombocytes on the 8th and 21st day after irradiation. No changes could be found in determining adhesiveness, platelet aggregation caused by ADP, and PF3A and PF3F tests. In the course of additional investigations (coagulation time in unprepared and siliconized glass tubes, thromboelastogramme, activated partial chromboplastine time), significant changes of coagulation time could be observed in siliconized glass tubes on the 8th, 11th, 21st, and 56th day following irradiation.
BACKGROUND: We investigated the suitability of two commercially available in-vitro bleeding tests (IVBT), the PFA-100 and the Hepcon HMS, to predict blood loss following operations with extracorporeal circulation (ECC) and compared them with conventional coagulation studies. METHODS: In 40 patients subjected to elective open heart surgery with ECC a blood sample was taken before and after ECC to measure platelet count, prothrombin time, aPTT, D-dimers, fibrinogen, and PFA-100 and Hepcon HMS data. The postoperative blood loss was recorded hourly until removal of drains. RESULTS: A significant correlation was found between total blood loss (250-1750 ml) and the preoperative PFA-100 (r = 0.41, p = 0.022), the preoperative platelet count (r = -0.42, p = 0.007), the preoperative D-dimer concentration in the plasma (r = 0.41, p = 0.01), and duration of ECC (r = 0.35, p = 0.044). There was no significant correlation between blood loss and the Hepcon HMS system. CONCLUSIONS: Although a significant correlation was found between blood loss and the PFA-100 IVBT, the practical value of these tests in the clinical situation is limited due to a great variability in individual results.
Procollagen-induced platelet aggregation, platelet retention (Hellem II), and platelet factor 3 availability (PF-3) were determinded in a group of healthy volunteers,acetylsalicylic acid (ASA) treated patients and in uraemic patients. ASA ingestion did not influence platelet retention and PF-3 availability. Uraemic patients had apronounced decrease in platelet aggregation and retention and PF-3 availability revealed inconsistent alterations. The relevance of the tests and the benefit of an ASA treatment for prophylaxis of thrombosis in Climino fistulae are discussed.
Aspirin (acetylsalicylic acid) is one of the main therapeutics in prevention of thrombo-embolic vascular events. Its efficiency is proved in the prevention of cardiovascular events. However, antiplatelet effect of aspirin is not absolute in all patients and some patients experience thrombo-embolic events despite aspirin. These patients are clinically called as aspirin resistant or aspirin non-responders. Globally, a lot of people are affected by aspirin resistance according to the high prevalence of athero-thrombotic vascular diseases. A prevalence of 5.5-45% in patients with various cardiovascular disease by different laboratory methods has been reported for aspirin resistance. Clinical outcome of aspirin resistance has been demonstrated in patients with different vascular diseases. Detection of platelet function in patients treated with aspirin may be necessary in the prediction of clinical outcome. Point of care methods, which have correlated results with the standard light transmittance aggregometry may be appropriate choices in the detection of platelets' response to antiplatelet therapy. Adequate additional therapies may reduce atherothrombotic risks and major cardiovascular events rate in aspirin resistant subjects. None of the current researches advised the cessation of aspirin therapy. There is need to investigate the efficacy of additional adenosine diphosphate receptor antagonists or newer antiplatelet agents in aspirin resistant subjects. The intent of this paper is to review the literature discussing possible mechanisms, determination techniques, and clinical effects of aspirin resistance.
Blood samples from 42 newborns, 78 infants and schoolchildren, and 81 healthy adults were tested for the parameters of primary hemostasis. Only whole blood techniques were used. Agonist-induced aggregation and release-reaction studies were performed in a whole blood lumi-aggregometer simultaneously. The release of adenosine triphosphate (ATP) was detected by the luciferin-luciferase method. The in vitro bleeding time was measured by the PFA 100 system. The results of these studies were ostensibly influenced by blood cells. Many aggregation phenomena were correlated with the platelet count. Aggregation and release reaction by collagen were inversely correlated with the hematocrit. In the PFA 100, hematocrit and leukocyte count were also inversely correlated with the closure time and the maximal blood flow velocity. Both parameters were diminished in newborns. The aggregation response to adenosine diphosphate (ADP) was similar in the three groups. The same was true for the aggregation and release reaction by arachidonic acid and for the agglutination by ristocetin. The aggregation and release reaction by collagen were diminished in the specimens from newborns. For the explanation of this transient hypofunction, only theoretical considerations exist. Beyond the postnatal period and during childhood, no remarkable differences from the adult norm were found.
Explore the source record for details and available documents.
Men have significantly more atherosclerotic disease than women. Platelet-mediated thrombosis plays a role in the initiation of myocardial infarction and stroke. Citrated whole blood from male and female donors was perfused through an annular system over everted human umbilical artery segments. Comparisons were made between platelet adherence and thrombus formation on subendothelium, platelet aggregation in citrated whole blood, hematologic variables, and the bleeding time. Platelet spreading and adherence were approximately 22% greater with male blood (P < 0.001), whereas thrombus formation on subendothelium and collagen- and arachidonic acid-induced platelet aggregation did not show sex-related differences. Platelet aggregation with adenosine diphosphate was greater in women, related to their lower hematocrit values. By contrast, in women hematocrit values showed a slight but significant positive correlation with platelet adherence on subendothelium. Fibrinogen was significantly correlated with collagen- and adenosine-diphosphate-induced platelet aggregation and with platelet adherence, spreading, and thrombus formation on subendothelium. The mean bleeding time was slightly longer in women than in men (P = 0.118). Platelet aggregation was not associated with the bleeding time except for collagen-induced platelet aggregation in males; the latter was significantly correlated with platelet adherence and spreading in both sexes, while arachidonic acid-induced platelet aggregation predicted platelet adherence and spreading in males. Male blood shows enhanced primary hemostatic activity; this may predispose men to atherosclerosis.