Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Platelet Function Tests”

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.

At least 217 records · Page 12Linked to original sources

Role of the retention test Homburg in evaluating platelet hyperactivity and in monitoring therapy with antiplatelet drugs.

Decreased retention in the retention test Homburg (RTH) indicates a loss of platelet function; increase is associated with an increased activation of platelets, for example, in patients with vascular diseases. Compared with other materials (e.g., collagen, glass pearls, etc.) the filter surface in the retention tubes is nonthrombogenic. Therefore, the RTH seems to be well suited for measuring an in vivo over-reactivity of platelets. In a pilot study using the RTH we evaluated the postoperative over-reactivity of platelets in 14 patients and observed a significant heterogeneity of the platelet population concerning size and stickiness. Reliable platelet function tests are also necessary for "drug monitoring," since they deliver important clinical laboratory parameters for efficient control of a therapy with antiplatelet drugs. Therefore, we evaluated in vitro how, after administration of platelet aggregation-inhibiting medications (such as acetylsalicylic acid, Prostaglandin and ReoPro in various concentrations, the adenosine diphosphate (ADP), collagen, ristocetin, or suprarenin increased retention can be reduced. The reaction of the platelets in platelet-rich plasma of different patients or donors to the addition of ADP is variable. The platelet function inhibitor effect is dose dependent. In a clinical pilot study, a significant platelet-inhibiting effect of clopidogrel using the RTH has been shown.

Abciximab↗

Atorvastatin reduces the ability of clopidogrel to inhibit platelet aggregation: a new drug-drug interaction.

BACKGROUND: We observed that the prodrug clopidogrel was less effective in inhibiting platelet aggregation with coadministration of atorvastatin during point-of-care platelet function testing. Because atorvastatin is metabolized by cytochrome P450 (CYP) 3A4, we hypothesized that clopidogrel might be activated by CYP3A4. METHODS AND RESULTS: Platelet aggregation was measured in 44 patients undergoing coronary artery stent implantation treated with clopidogrel or clopidogrel plus pravastatin or atorvastatin, and in 27 volunteers treated with clopidogrel and either erythromycin or troleandomycin, CYP3A4 inhibitors, or rifampin, a CYP3A4 inducer. Atorvastatin, but not pravastatin, attenuated the antiplatelet activity of clopidogrel in a dose-dependent manner. Percent platelet aggregation was 34+/-23, 58+/-15 (P=0.027), 74+/-10 (P=0.002), and 89+/-7 (P=0.001) in the presence of clopidogrel and 0, 10, 20, and 40 mg of atorvastatin, respectively. Erythromycin attenuated platelet aggregation inhibition (55+/-12 versus 42+/-12% platelet aggregation; P=0.002), as did troleandomycin (78+/-18 versus 45+/-18% platelet aggregation; P<0.0003), whereas rifampin enhanced platelet aggregation inhibition (33+/-18 versus 56+/-20% platelet aggregation, P=0.001). CONCLUSIONS: CYP3A4 activates clopidogrel. Atorvastatin, another CYP3A4 substrate, competitively inhibits this activation. Use of a statin not metabolized by CYP3A4 and point-of-care platelet function testing may be warranted in patients treated with clopidogrel.

Adolescent↗

Use of a platelet filter test in patients with thrombocytosis.

In the differential diagnosis of primary and secondary thrombocytosis platelet function tests may play an important role. We examined the applicability of a platelet filter test (shear-dependent platelet aggregation) as a tool, to differentiate primary thrombocytosis (cases with myeloproliferative disorders) from secondary (reactive) thrombocytosis. The test was carried out in 53 patients suffering from myeloproliferative disorders associated with primary thrombocytosis and in 21 patients with other diseases complicated by secondary thrombocytosis. Using citrate as anticoagulant, the sensitivity of the O'Brien's test proved to be 77.1%, and its specificity 94.4%. Using heparin as anticoagulant the sensitivity and specificity of the test were found to be also reliably high. Based on these studies we suggest the use of the O'Brien's filterometer as a screening test in the differential diagnosis in patients with elevated platelet count. In the case of normal results, the causes of reactive thrombocytosis should be clarified first, while with abnormal results, haematological examination of the patients should be performed.

Adenosine Diphosphate↗

Presence of factors that activate platelet aggregation in mitral stenotic patients' plasma.

BACKGROUND: Although the association between mitral stenosis (MS) and increased coagulation activity is well recognized, it is unclear whether enhanced coagulation remains localized in the left atrium or whether this represents a systemic problem. To assess systemic coagulation parameters and changes in platelet aggregation, we measured fibrinogen levels and performed in vitro platelet function tests in plasma obtained from mitral stenotic patients' and from healthy control subjects' peripheral venous blood. METHODS: Sixteen newly diagnosed patients with rheumatic MS (Group P) and 16 healthy subjects (Group N) were enrolled in the study. Platelet-equalized plasma samples were evaluated to determine in vitro platelet function, using adenosine diphosphate (ADP), collagen and epinephrine in an automated aggregometer. In vitro platelet function tests in group N were performed twice, with and without plasma obtained from group P. RESULTS: There were no significant differences between the groups with respect to demographic variables. Peripheral venous fibrinogen levels in Group P were not significantly different from those in Group N. Adenosine diphosphate, epinephrine and collagen-induced platelet aggregation ratios were significantly higher in Group P than in Group N. When plasma obtained from Group P was added to Group N subjects' platelets, ADP and collagen-induced, but not epinephrine-induced, aggregation ratios were significantly increased compared to baseline levels in Group N. CONCLUSION: Platelet aggregation is increased in patients with MS, while fibrinogen levels remain similar to controls. We conclude that mitral stenotic patients exhibit increased systemic coagulation activity and that plasma extracted from these patients may contain some transferable factors that activate platelet aggregation.

Journal Article↗

Impact of Race on Profiles of Platelet Reactivity and Clinical Outcomes in Clopidogrel-Treated Participants.

Black individuals undergoing percutaneous coronary intervention (PCI) experience higher rates of major adverse cardiovascular events (MACE) than non-Black individuals. This study assessed the racial differences in platelet reactivity and clinical outcomes among clopidogrel-treated participants. Two cohorts were analyzed. The pharmacodynamic (PD) cohort involved patients with atherosclerotic cardiovascular disease on maintenance clopidogrel therapy undergoing platelet function testing. The primary outcome was high platelet reactivity (HPR, i.e., P2Y12 reaction unit [PRU]&#x2009;>&#x2009;208). The PCI cohort included participants undergoing PCI on clopidogrel-based dual antiplatelet therapy. The primary outcome was 1-year MACE, defined as the composite of cardiovascular death, myocardial infarction (MI), ischemic stroke, or stent thrombosis. Data on clinically significant bleeding and CYP2C19 genotyping alleles were collected. The PD and PCI cohorts included 728 (32.1% Black) and 2,770 (20.5% Black) participants, respectively. Black participants had higher PRU levels (184 [IQR 128-234] vs. 144 [IQR 88-195]; P&#x2009;<&#x2009;0.001) and higher prevalence of HPR (39.3% vs. 20.6%; P&#x2009;<&#x2009;0.001). Independent predictors of HPR included Black race, hemoglobin levels, and presence of CYP2C19 loss-of-function allele. In the PCI cohort, Black participants had a higher risk of MACE (HR 1.47; 95% CI 1.02-2.11; P&#x2009;=&#x2009;0.037), primarily driven by MI (HR 1.71; 95% CI 1.09-2.67; P&#x2009;=&#x2009;0.019), with no significant difference in clinically significant bleeding (HR 1.08; 95% CI 0.65-1.80; P&#x2009;=&#x2009;0.768). Black participants on clopidogrel exhibit higher platelet reactivity, increased rates of HPR, and an elevated risk of MACE within 1 year after PCI, without significant differences in bleeding compared to non-Black participants.

Aged↗

Platelet scintigraphy and survival in juvenile stroke patients.

In the present study the prevalence of active atherosclerotic lesion sites in the carotid and femoral arteries as well as the platelet survival in a selected group of 33 patients (8 males, 25 females) below the age of 50 after juvenile stroke has been examined. In the patients studied a high frequency (80%) of positive (visible) carotid artery lesions with a platelet uptake ratio (PUR) ranging from 1.07-1.79 as well as an extremely shortened platelet survival were monitored. In-vitro platelet function tests, however, did not show significant abnormalities. No correlation between PUR, platelet survival, platelet function and the clinical situation could be assessed. These findings indicate that in this highly selected group of patients in-vivo haemostatic balancing seems to be severely impaired.

Adult↗

Anti-thrombotic effect of strawberries.

Because of the high mortality, prevention of arterial thrombotic disease has top priority in developed countries. As inappropriate diet is known to predispose to acute thrombotic events, regular intake of an anti-thrombotic diet may offer a convenient and effective method of prevention. As part of a systematic investigation into the anti-thrombotic effect of fruits and vegetables, strawberry varieties were tested in this study. An in vitro platelet function test (haemostatometry) was used for screening strawberry filtrates. Those that showed significant antiplatelet effect were further assessed with a laser-induced thrombosis test in mice. Measurement of flow-mediated vasodilation in the femoral artery of mice reflected the effect on the vascular endothelium. Correlation between the effects on platelet reactivity in vitro and the antioxidant activity (hypoxanthine/xanthine oxidase test) or phenolic compound content was assessed. Strawberry varieties KYSt-4 (Nohime), KYSt-11 (Kurume IH-1) and KYSt-17 (Kurume 58) showed significant antiplatelet activity both in vitro and, after oral administration, in vivo. Both KYSt-11 and KYSt-17, but not KYSt-4, significantly reduced flow-mediated vasodilation; that is, caused endothelial dysfunction. Antiplatelet activities were heat stable. Significant correlation was found between antiplatelet and antioxidant activities (P=0.049, R=0.23) or total phenolic compounds (P=0.0096, R=0.36). Of the tested strawberry varieties, KYSt-4, KYSt-11 and KYSt-17 showed significant anti-thrombotic effect. The dual mechanism of the effect may involve a direct inhibition of both platelet function and antioxidant activities.

Animals↗

Limited early antiplatelet effect of 300 mg clopidogrel in patients with aspirin therapy undergoing percutaneous coronary interventions.

AIM: Our aim was to evaluate the early efficacy and variability of the platelet inhibition exerted by 300 mg clopidogrel for the purpose of acute percutaneous coronary interventions using platelet function tests. METHODS AND RESULTS: Elective percutaneous coronary intervention was used as a timely model in which clopidogrel was added to ongoing acetylsalicylic acid (aspirin) (100 mg/day) at 2.5 h prior to procedure. Blood samples were collected before administration of clopidogrel and immediately before the intervention from 50 patients. Platelet functions were assessed with traditional aggregation and PFA-100. At baseline, 14 (28%) patients were poor responders to aspirin according to PFA and 9 (18%) continued to show arachidonic acid-induced aggregation. After clopidogrel ADP-triggered aggregation was only modestly inhibited in 40% of the patients. Eight percent of the study population was left without any measurable antiplatelet effect. The patients with modest response to clopidogrel had higher levels of c-peptide (1.5 nmol/L) than the ones responding well (0.9 nmol/L, P<0.05). CONCLUSION: Neither ongoing aspirin treatment nor added clopidogrel did reach an expected extent of platelet inhibition. This study shows that aspirin-treated patients undergoing PCI gain highly variable levels of platelet inhibition with short-term clopidogrel 300 mg. At 2 h after adding clopidogrel it failed to enhance platelet inhibition in 40% of the patients. In future, targeted platelet function tests may be helpful to individually select an effective antiplatelet medication for these patients. This study suggests that for acute PTCA clopidogrel does not reach the optimal antithrombotic efficacy in all patients.

Adult↗

[Point-of-care testing of hemostatic alterations in anaesthesia and intensive care].

In recent years point-of-care testing (POCT) has seen wider applications in the clinical management of surgical and critically ill patients. The available methods for haemostasis analysis include simple-to-handle tests for the assessment of plasmatic coagulation, platelet function tests and the more complex visco-elastic assays. The main advantage of POCT is the fast availability of the results allowing a targeted management of haemostasis disorders. The benefits and risks of POCT depend on the urgency of the analysis, the turn-around time of the laboratory tests, the availability of motivated staff at the point-of-care and the expected haemostatic alterations. An underestimated aspect of POCT is the importance of established quality management procedures. For this purpose control materials based on plasma or artificial fluids are being applied. In spite of often higher costs we appraise the use of POC analysis in many settings as justified because of the gain of time and the overall better process quality, i.e. targeted haemostasis therapy instead of consecutive application of different therapeutic options.

Anesthesia↗

Ecchymoses: an unusual manifestation of toxocariasis in children.

OBJECTIVE: To investigate the aetiology of multiple ecchymoses associated with eosinophilia. SETTING: Professorial Paediatric Unit (PPU) at Lady Ridgeway Hospital (LRH) for children, Colombo. DESIGN: Prospective study from July 1998 to April 2000. MATERIALS AND METHODS: Patients admitted to the PPU with multiple ecchymoses associated with an absolute eosinophilia (> 1 x 10(9)/1) were investigated further to determine the possible aetiology; bleeding time, clotting time, platelet count, platelet function tests, stools examination and toxocara antibody tests were performed. Patients who were positive for toxocara were treated either with thiabendazole or albendazole. Patients who had geohelminth infestations were treated with mebendazole. RESULTS: 14 children (11 boys) were studied. 7 were between 1 and 5 years, and 7 were above 5 years of age. The mean eosinophil count was 4.3 x 10(9)/1. All patients had a prolonged bleeding time, but clotting time and platelet counts (mean value 220 x 10(9)/1) were normal. Platelet function tests were done in 5 patients. Twelve patients were positive for toxocariasis and the other 2 were positive for ascariasis. All children who were positive for toxocariasis had contact with pet cats or dogs. Six patients were treated with thiabendazole and 6 with albendazole. The two patients who had ascariasis were treated with mebendazole. Post-treatment mean eosinophil count was 0.63 x 10(9)/1, and the bleeding time was 4 minutes. CONCLUSION: Toxocariasis could present with ecchymoses due to an acquired bleeding disorder. Awareness of this would help to investigate, diagnose and treat early, and lessen parental anxiety.

Child, Preschool↗

The effect of ICI 55,897 and clofibrate on platelet function and other tests abnormal in atherosclerosis.

There is considerable evidence that the quantity or quality of plasma lipids influences platelet function tests, and clofibrate reduces high plasma lipids and alters some platelet tests. Clofibrate was accordingly given to patients with vascular disease who were at risk of thrombosis. The heparin thrombin clotting time (HTCT), initially short and thus possibly reflecting increased activation, was regularly returned to normal after about a month's delay. The fibrinogen was also normalized but the initially abnormal anti-thrombic activity became more abnormal. ICI 55,897, an analogue of clofibrate, also normalized the HTCT and the fibrinogen and had no adverse effect on the anti-thrombin levels. This compound has no effect on plasma lipids. If it can be shown that the correction of abnormal tests conveys clinical benefit these findings suggest that ICI 55,897 might clinically be more beneficial than clofibrate. However, direct comparison of clofibrate and ICI 55,897 suggests that clofibrate is more effective in normalizing the HTCT. The mechanism underlying these drug-induced changes are unknown but they cannot be directly related to lipid changes.

Aged↗

EDTA dependent pseudothrombocytopenia caused by antibodies against the cytoadhesive receptor of platelet gpIIB-IIIA.

AIMS: To clarify the mechanisms involved in the development of EDTA dependent pseudothrombocytopenia, particularly the platelet receptors. METHODS: Platelets were measured in 33 patients with pseudothrombocytopenia, using different anticoagulants to collect blood samples (direct test). The results were compared with the counts obtained by adding patients' serum or immunoglobulins to normal blood samples (indirect test). The role of platelet function was explored using ASA, PGE1, and apyrase as platelet inhibitors. The contribution of platelet receptor/s was investigated using antigens to gpIb-IX and gpIIb-IIIa monoclonal antibodies. Immunoglobulin class was estimated by the ability of IgG, IgA, and IgM antibodies to prevent platelet clumping. RESULTS: Agglutinating antibodies were IgA in 40%, IgG in 30%, and IgM in 10% of patients studied. Both patients' serum and immunoglobulins induced platelet clumping in normal samples anticoagulated with EDTA (indirect test). This was prevented by incubation of blood samples at 37 degrees C and almost completely inhibited by the platelet inhibitors ASA, PGE1, and apyrase. Pseudothrombocytopenia was also entirely prevented by an antigen to gpIIb-IIIa monoclonal antibody that recognises fibrinogen and the von Willebrand factor binding site. Pseudothrombocytopenia was almost completely abolished after the addition of RGD peptide, the recognition sequence of cytoadhesive proteins. CONCLUSIONS: These findings suggest that EDTA dependent pseudothrombocytopenia is caused by agglutinating antibodies that recognise cytoadhesive receptors on platelet gpIIb-IIIa and that an efficient platelet metabolism is required.

Adult↗

Low molecular weight heparin as an anticoagulant for in vitro platelet function studies.

We evaluated the suitability of low molecular weight (LMW) heparin as an anticoagulant for in vitro platelet function tests in 11 normal volunteers. Results with citrated platelets were considered as the standard. Spontaneous platelet aggregation and the aggregation responses to ADP, epinephrine, collagen, ristocetin and thrombin were measured turbidimetrically in an aggregometer. Dose-response and dose-rate curves were constructed for ADP- and epinephrine-induced aggregation. The maximum aggregation response (EDmax) and rate (EDRmax), and the estimated dose of agonist to induce 50% of the maximum response (ED50) and rate (EDR50) were calculated from these curves. The inhibition of ADP-induced aggregation with PGI2 was expressed as per cent inhibition. The release of ATP and TxA2, from platelets aggregated with collagen was measured. No spontaneous aggregation occurred with either anticoagulant. The ED50 and the EDR50 for heparinized platelets were significantly lower for ADP induced aggregation (0.8 +/- 0.3 microM vs 2.1 +/- 1.0 microM [p = 0.001] and 0.4 +/- 0.1 microM vs 0.8 +/- 0.3 microM [p = 0.003]). The EDRmax with ADP was significantly higher (p = 0.004) for heparinized platelets (64.6 +/- 17.0 units/ml vs 50.4 +/- 7.6 units/ml). The heparinized platelets aggregated slightly, but significantly, less in response to ristocetin than the citrated platelets. The response of washed heparinized and citrated platelets to thrombin was not significantly different. The per cent inhibition of ADP aggregation with PGI2, was significantly lower with heparinized platelets. The release of TxA2 and ATP was similar for both anticoagulants. These results indicate that LMW heparin is a satisfactory anticoagulant for platelet aggregation tests.

Adenosine Diphosphate↗

Inherited haemorrhagic disease with abnormal prothrombin consumption.

The propositus is a 4-year-old boy who presented with a history of excessive bleeding after surgical procedures as well as haematomas and epistaxis. The defect in haemostasis consisted in an anomaly of the prothrombin consumption tests as the only abnormality while all the other conventional coagulation and fibrinolysis tests as well as platelet function tests were normal. The father of the propositus had no previous history of excessive bleeding but was found to have an abnormal prothrombin consumption index. The reaction to prothrombin conversion, normal at onset, slowed down to less than normal and did not reach completion until 24 h. The in vivo studies suggest that the effect does not act on the interaction between platelet phospholipid and plasma. The factor II dosage and the electrophoretic mobility of prothrombin of the plasma were normal; nevertheless when studying the purified prothrombin by means of crossed immunoelectrofocusing there appeared an anomaly of pI. This result suggests the possible existence of an abnormal prothrombin molecule responsible for a slow prothrombin conversion.

Blood Coagulation Disorders↗

Comparison of the effects of transfusions of cryopreserved and liquid-preserved platelets on hemostasis and blood loss after cardiopulmonary bypass.

OBJECTIVE: The aim of the study was to compare the clinical effects and hemostatic efficiency of transfusions of platelets preserved in the frozen state for as long as 2 years with transfusions of platelets preserved in the conventional manner for as long as 5 days in patients undergoing cardiopulmonary bypass. METHODS: Seventy-three patients were prospectively randomly assigned to receive transfusions of cryopreserved or liquid-preserved platelets. Nonsurgical blood loss was measured during and after the operation. Bleeding time, hematologic variables, and the bleeding time site shed blood were assayed before cardiopulmonary bypass and at 30 minutes and 2, 4, and 24 hours after transfusion. In vitro platelet function tests were conducted on platelets obtained from healthy volunteers. RESULTS: No adverse sequelae of the transfusions were observed. Blood loss and the need for postoperative blood product transfusions were lower in the group receiving cryopreserved platelets. Lower posttransfusion platelet increments and a tendency toward decreased platelet survival were observed in patients receiving cryopreserved platelets. Hematocrit and plasma fibrinogen were significantly higher in this group, and the duration of intubation was shorter. In vitro, cryopreserved platelets demonstrated less aggregation, lower pH, and decreased response to hypotonic stress but generated more procoagulant activity and thromboxane. CONCLUSIONS: (1) Cryopreserved platelet transfusions are superior to liquid-preserved platelets in reducing blood loss and the need for blood product transfusions after cardiopulmonary bypass. (2) The reduction in blood loss in the patients receiving cryopreserved platelet transfusions after cardiopulmonary bypass probably reflects improved in vivo hemostatic function of cryopreserved platelets. (3) Some in vitro measures of platelet quality (aggregation, pH, hypotonic stress) may not reflect in vivo quality of platelet transfusions after cardiopulmonary bypass, whereas other in vitro measures (platelet procoagulant activity and thromboxane) do.

Aged↗

Determination of the density distribution of human platelets--methodological aspects and comparison with other tests for platelet activation.

Stimulation of human platelets to release results in decreased buoyant density. This decreased density provides a tool to detect circulating platelets which have participated in a thrombotic process. Platelet density gradient centrifugation using Stractan was standardized and the effects of anticoagulation, temperature, and osmolarity were investigated. In 7 out of 32 patients with thrombotic disease less dense platelets were found. Platelet activation in the patient group was also indicated by spontaneous aggregation (10/32), decreased circulating platelet aggregate ratios (5/24) and elevated plasma beta-thromboglobulin levels (2/ 11). Several of these tests were also abnormal in diabetes mellitus thrombocytosis, leukaemia and several systemic diseases with thrombotic complications. The platelet density test using Stractan is reproducible and independent of other tests for platelet activation and is therefore potentially a useful extension of platelet function testing in patients with thrombotic disease.

Adult↗

Platelet function point-of-care tests in post-bypass cardiac surgery: are they relevant?

BACKGROUND: Platelet dysfunction is an important cause of excessive bleeding after cardiac surgery. We assessed two platelet function point-of-care tests: the platelet function analyser (PFA-100) and the Hemostatus(TM) in patients with and without excessive bleeding after cardiac surgery with cardiopulmonary bypass. METHODS: Mediastinal chest tube drainage (MCTD) was measured for the first 6 h in the intensive care unit (ICU). Haematology and coagulation tests were done on arrival in the ICU, and when excessive bleeding occurred (MCTD >1 ml kg(-1) h(-1)) or after 3 h. RESULTS: Eighteen patients bled excessively and 27 had normal MCTD. Hemostatus measurements were prolonged in those with excessive bleeding compared with the normal group. The times for PFA-100 adenosine diphosphate (ADP) and epinephrine were 91 vs 71 s (P=0.004) and 155 vs 114 s (P=0.02) in the bleeding and normal group s, respectively. None of the Hemostatus or PFA-100 values correlated with total MCTD. Depending on the agonist used, maximum aggregation was 33-81% and 52-86% in bleeding and normal groups, respectively. Only poor correlations were found between PFA-100 epinephrine and maximum aggregation in response to ADP (r=-0.52, P=0.03) or to collagen (r=-0.48, P=0.04). CONCLUSION: Patients bleeding excessively in the ICU had abnormal measurements in point-of-care tests without a dramatic decrease in aggregation. Except for patients with increased risk of postbypass bleeding, point-of-care tests are not useful for routine use after cardiac surgery.

Aged↗

The sensitivity of tests to detect in vivo platelet activation induced by the removal of arterial endothelium of the baboon (Papio ursinus).

The relative sensitivities for the various in vivo and in vitro tests for platelet activation are unknown. This was studied in a baboon model where limited and more substantial injury to the vascular endothelium was inflicted. The endothelium of a segment of the right carotid artery was removed with a balloon catheter on day 0 (limited de-endothelialisation), and that of the left carotid artery, abdominal aorta and left femoral artery on day 7 (substantial de-endothelialisation). Eight baboons (Papio ursinus) were used. Baseline tests for platelet activation (platelet volume, platelet density, platelet aggregate ratio, and platelet and plasma levels of platelet factor 4 [PF4] and beta-thromboglobulin [beta-TG]) were performed 7 days before de-endothelialisation and repeated on days 1, 9 and 16. The kinetics of indium-111-labelled platelets were measured after substantial de-endothelialisation. Sham operations were done on 3 animals exactly as in the test, except that the balloon injuries were not inflicted. No influence on the results of the platelet function tests was found. The only test capable of detecting limited injury to the endothelium was the measurement of plasma PF4. The mean platelet life-span (MPLS) shortened, mean platelet density decreased, the circulating platelet aggregate ratio decreased, and plasma levels of PF4 and beta-TG increased (P less than 0.05 in all instances) after the substantial endothelial injury. The mean platelet volume, intraplatelet PF4 and beta-TG, and the in vivo distribution and sites of sequestration of labelled platelets were poor tests for in vivo platelet activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗