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At least 1,135 records · Page 63Linked to original sources
PubMed1991

The platelet-reactivity-test--a useful "by-product" of the blood-sampling procedure?

Blood sampling demands the insertion of a needle into the blood-vessel thereby causing a destruction of the endothelial wall of the blood-vessel. The physiological reaction of platelets is the occlusion of endothelial lesions. Reaction of platelets induced by endothelial lesions lasts about 10 ms. Each blood sampling procedure should therefore activate platelets. A simple platelet test-system was designed following these considerations. Blood samples were collected twice, in EDTA-buffer and in EDTA-formalin-buffer. Activated (aggregated) platelets were fixed by formalin or dissolved in EDTA-buffer. Platelet-reactivity (PR) was calculated as quotient of the number of platelets remaining in the supernatant of both samples after centrifugation. The PR-index-values strongly depended on the blood-sampling procedure. Standardization of the blood sampling procedure led to normal distributed PR-index-values in 110 healthy controls (0.98 +/- 0.09). PR-index-values remained constant during a period of 260 days. PR-index-values in 49 patients suffering from encephalomyelitis disseminata were 1.04 +/- 0.15 and 1.64 +/- 0.6 in 72 patients suffering from transitoric ischemic attacks. Differences between healthy controls and patients suffering from TIA's were significant (p less than 0.001).

Adult↗
PubMed1983

Platelets and diabetic vascular disease.

Tests of platelet behaviour in vitro, particularly aggregation and retention and in vivo tests such as measurement of platelet survival and plasma levels of beta-thromboglobulin are frequently abnormal in diabetic patients, particularly in those with vascular disease. The concept has therefore arisen that platelet hyper-reactivity is one factor responsible for diabetic microangiopathy. Whereas there is experimental and histological evidence for the mediation of platelets in the pathogenesis of atherosclerosis, direct evidence of platelet involvement in microangiopathy is scanty. Similar alterations in platelet behaviour have been observed in a variety of other conditions with vessel wall damage in common and evidence is presented which suggests that these platelet abnormalities may be secondary to vessel wall injury. In diabetic subjects, some changes in platelet behaviour are reversed by improved glycaemic control. Evidence that platelets are involved in the pathogenesis of diabetic microangiopathy therefore remains circumstantial, though current trials of anti-platelet agents may enable a more precise evaluation of their role.

Adenosine Diphosphate↗
PubMed1995

Heparin-induced thrombocytopenia: an improved method of detection based on lumi-aggregometry.

Heparin-induced thrombocytopenia (HIT) is a recognized complication of heparin administration. Early detection of this syndrome is essential in the prevention of immune-mediated thromboembolic sequelae. The 14C-serotonin release assay (SRA) has been used in reference laboratories to identify sera from patients on heparin therapy capable of inducing platelet dense granule release. In an attempt to improve existing methodologies, we employed luminographic detection of platelet-dense granule ATP release as an endpoint of HIT antibody-mediated platelet activation. Sera tested included 10 SRA confirmed positive and five SRA confirmed negative samples (to establish the assay), five samples from patients with thrombocytopenia not on heparin therapy and 34 patients suspected of HIT syndrome. All SRA confirmed positive sera (n = 19) were positive by the luminographic procedure. 24/26 SRA confirmed negative sera and five sera from thrombocytopenic patients not on heparin therapy were negative using luminography. Two of four sera yielding equivocal SRA results were found to be positive by the luminographic technique. The data suggest that the use of a lumiaggregometer in the coagulation laboratory to detect HIT antibody-induced platelet activation is a reliable alternative to the SRA. The luminographic procedure is both rapid and sensitive, and does not require the use of biohazardous radio-isotopes.

Adenosine Triphosphate↗
PubMed2006

The Retention Index Test Homburg (RTH-II): Response to clopidogrel and comparison with aggregometry and CD62P-expression.

The Retention Index Test Homburg (RTH-II) is quoted to detect effects of shear stress on platelets, which involve ADP receptor signaling. RTH-II might be a tool for monitoring antiplatelet therapy for compounds that interfere with ADP induced platelet activation and secretion. In a series of investigations, we used an ADP (2 microM) triggered RTH-II in parallel with light-transmittance aggregometry and flow cytometry in subjects before and after clopidogrel. A loading dose of 225 mg clopidogrel leads to a significant reduction (p < 0.01) in the ADP-stimulated retention index (RI) from 69 +/- 15 to 48 +/- 21%, in the aggregation response to 5 microM ADP (from 50 +/- 20 to 29 +/- 21%) and the expression of CD62P (from 64 +/- 11 to 41 +/- 17%). Correlation analysis showed that the RI corresponds significantly to CD62P-expression (p < 0.01) but not to aggregation. We also found a strong correlation (p < 0.01) between the ADP-stimulated RI and the expression of CD62P after stimulation with 2 microM ADP, whereas no correlation was seen for RI vs. binding of PAC-1 or aggregation. Platelets not retained in the filter had lower CD62P expression than measured in the sample before the filter passage (54 vs. 35%). A direct interaction of CD62P with platelet ligands might lead to enhanced retention in RTH and explain the correlation of RI with CD62P expression. The RTH-II might be a simple and easy to handle platelet function assay for monitoring effects on P2Y(12)-inhibitors on platelet degranulation, perhaps in addition to aggregometry.

Adenosine Diphosphate↗
PubMedDate not supplied

Nonsteroidal anti-inflammatory drugs and aspirin: a comparison of the antiplatelet effects.

Antiplatelet effects of common analgesics were assessed in vitro. The Streck Platelet Aggregation Test Kit (Omaha, NE) was used to measure percent platelet aggregation in response to sodium arachidonate, collagen, adenosine diphosphate, and ristocetin in patients on various analgesics. In comparison with the control group, the response to arachidonate and collagen of ibuprofen (86% vs. 33% and 55% vs. 23%), naproxen (86% vs. 43% and 55% vs. 29%), indomethacin (86% vs. 26% and 55% vs. 17%), and aspirin (86 vs. 21% and 55 vs. 23%) all demonstrated a significant yet comparable reduction in platelet aggregation (p < 0.01). Because of the comparable antiplatelet effects of aspirin and NSAIDs, the additional benefits of daily aspirin in those patients on chronic and consistent NSAID therapy must be reconsidered.

Adult↗
PubMed1995

Platelet unresponsiveness to collagen: involvement of glycoprotein Ia-IIa (alpha 2 beta 1 integrin) deficiency associated with a myeloproliferative disorder.

We studied a 66-year-old man with a myeloproliferative disorder who presented with a prolonged bleeding time and marked thrombocytosis (platelet count, 3,890 x 10(9)/l). There was no past history of a bleeding disorder. The patient had normal coagulation data. His platelets completely lacked collagen-induced platelet aggregation and adhesion, but showed normal responses to other agonists. All family members tested showed normal platelet aggregation with collagen. Analysis of 125I surface-labeled platelets by two-dimensional SDS gel electrophoresis disclosed absence of the spot corresponding to platelet membrane GPIa (alpha 2) but no other significant deficiencies of major platelet glycoproteins i.e., GPIb, IIb-IIIa, and IV. Immunoisolation studies of the patient's platelets indicated that neither anti-GPIa nor anti-GPIIa (beta 1) monoclonal antibody (mAb) isolated any surface membrane proteins corresponding to GPIa. GPVI, a putative collagen receptor, was immunoisolated from the platelets. Indirect immunofluorescence study using flow cytometry confirmed that the patient's platelets were totally deficient in surface expression of the GPIa-IIa complex (alpha 2 beta 1 integrin). In contrast, phytohemoagglutinin-activated T-lymphocytes from the patient expressed normal concentrations of this complex. The data suggest that our patient had an acquired deficiency of the platelet GPIa-IIa complex, due to a myeloproliferative disorder, which might account for the absence of responsiveness of his platelet to collagen.

Acute Disease↗
PubMed1988

[Effect of cod liver oil administration on blood lipid levels, lipoprotein profile and bleeding time].

In a research study performed over eight months with five female and six male subjects (age 35-67 years) the effect of cod liver oil on the lipoprotein composition in the blood was tested. The main goal was to prove that the regular administration of so-called highly unsaturated omega-3-fatty acid components in fish oil (4 g per day over six months) may lead to a reduction of triglyceride and total cholesterol values. Furthermore, any changes in HDL and LDL cholesterol fractions as well as the bleeding time were registered. The average values of all subjects showed an essential reduction of the triglyceride and cholesterol values. The control examination after 8 months even showed a continuous trend. The LDL fractions on an average remained unchanged. It can be taken for granted that the administration of unsaturated fatty acids in cod liver oil shows a successful therapeutic effect by the reduction of triglyceride and cholesterol values. The anti-atherosclerotic and the anti-platelet aggregational effect of fish oil has been described in many publications.

Adult↗
PubMed1990

Attempts to standardize platelet aggregation measurements: simplified screening tests.

We present a standardized measurement of collagen and ADP-induced platelet aggregation with the help of a personal computer. The calculator improves the recording of measurements and the automatic calculation of parameters to define the strength of aggregation in various aggregation phases, as well as aggregation and disaggregation velocities. The dose-effect relationships between aggregants and five calculated parameters after addition of ADP and four after addition of collagen are demonstrated in the light of measurements taken in 40 healthy persons. Comparison of these measurements with those of 8 volunteers 24 h after they had taken 250 mg of acetylsalicylic acid and those of of 5 patients with typical illnesses associated with hypo- and hyperaggregability shows that analysis of the aggregation with two reagent concentrations (1, 2 and 4 micrograms/ml collagen, 1, 2 and 4 mumols/ml ADP) and the resulting values allow one to distinguish between normal, hypo- and hyperaggregable platelets.

Adenosine Diphosphate↗
PubMed2004

Significantly reduced spontaneous thrombolytic activity in older men: a possible explanation for the gender differences in risk of acute coronary syndromes.

BACKGROUND: Although incidence of arterial thrombotic events increases with advancing age, the mechanism of such increased risk is poorly understood. There is also a gender difference; coronary heart disease is more common in men than women. The aim of the present study was to investigate the possible contribution from platelet reactivity and spontaneous thrombolysis, determinants of arterial thrombosis, to the increased risk of thromboembolism in aging, but otherwise healthy subjects. METHOD: One hundred and forty-five normal subjects (61 men, 82 women) of age between 19 and 77 years were grouped into groups of young (<30 years); middle aged (31-50 years), and older (>51 years), according to their gender and body mass index (BMI). A new in vitro test [Gorog Thrombosis Test (GTT)] was used to measure in sequence both platelet reactivity [occlusion time (OT)] and spontaneous thrombolysis [lysis time (LT)] from one non-anticoagulated blood sample. RESULT: OT in all women was 315+/-9.2 s (mean+/-S.E.M.), in all men OT was 300+/-10.6 s. The mean LT in all women was 2557+/-201.5 s, and in all men LT was 2493+/-198.6 s. Advanced age did not enhance platelet reactivity (OT), but increased BMI did (P=0.039). Spontaneous thrombolysis (LT) was impaired in older men but not in women (difference between young vs. middle age: P=0.019; young vs. older: P=0.0002). CONCLUSION: Our findings suggest that in men, spontaneous thrombolytic activity is reduced with age, and this may explain the increased frequency and severity of thromboembolic events. Interestingly, in women, spontaneous thrombolytic activity did not change after menopause.

Acute Disease↗
PubMed2006

Evidence that pre-existent variability in platelet response to ADP accounts for 'clopidogrel resistance'.

BACKGROUND: Clopidogrel is a widely used antithrombotic agent that inhibits the platelet P2Y(12) adenosine diphosphate (ADP) receptor. There is increasing interest in 'clopidogrel resistance'. OBJECTIVES: To determine whether 'clopidogrel resistance' is accounted for by a pre-existent variability in platelet response to ADP. METHODS: Platelet response to 20 microm ADP was analyzed by four independent whole blood flow cytometric assays: platelet surface activated GPIIb-IIIa, platelet surface P-selectin, monocyte-platelet aggregates and neutrophil-platelet aggregates. In 25 consecutive, non-aspirin-treated healthy subjects, we studied platelet response before and after clopidogrel administration. In addition, we studied the platelet response in 613 consecutive aspirinated patients with or without coronary artery disease (CAD, as determined by angiography) who had or had not been treated with clopidogrel. In these patients, we tested for homogeneity of variance across all durations of clopidogrel exposure and severity of CAD by estimating the 'goodness of fit' of two independent models. RESULTS: In the healthy subjects, pre-clopidogrel response to ADP predicted post-clopidogrel response to ADP. In the patients, clopidogrel, as expected, inhibited the platelet response to ADP. However, irrespective of the duration of clopidogrel administration, the severity of CAD, and the dose of aspirin, clopidogrel did not increase the variance in the platelet response to ADP in any of the four assays of platelet response. CONCLUSIONS: These studies provide evidence that 'clopidogrel resistance' is accounted for by a pre-existent variability in platelet response to ADP and this variability is not increased by clopidogrel administration.

Adenosine Diphosphate↗
PubMed1989

Abnormal platelet aggregation in patients with Raynaud's phenomenon.

Platelet aggregation in vitro to several aggregating agents (serotonin (5-HT), adenosine diphosphate, adrenaline and collagen) was studied in 16 patients with primary and secondary Raynaud's phenomenon and compared with that in 13 normal volunteers. Platelets from patients with Raynaud's phenomenon had significantly greater responses to all the 5-HT concentrations tested (p less than 0.001 for 10 microM; p less than 0.01 for 1 microM; p less than 0.05 for 0.1 microM; p less than 0.02 for 0.025 microM) and to low doses of adenosine diphosphate (p less than 0.01 for 1 microM; p less than 0.02 for 0.5 microM) but normal responses to collagen, adrenaline, and high doses of adenosine diphosphate. Patients with secondary Raynaud's phenomenon were significantly more hypersensitive to 0.5 microM adenosine diphosphate than patients with primary Raynaud's phenomenon. In patients with secondary Raynaud's phenomenon there was a significant correlation between the extent of 5-HT aggregation and the duration of the disease. The finding that platelets from patients with Raynaud's phenomenon have enhanced responses to 5-HT and adenosine diphosphate, but normal responses to adrenaline and collagen, is consistent with a role for 5-HT in this disease.

Adenosine Diphosphate↗
PubMed2003

Impaired spontaneous thrombolytic activity in elderly and in habitual smokers, as measured by a new global thrombosis test.

We used a new test (the Görög Thrombosis Test) for assessing the effect of aging, smoking and exercise habits on the overall thrombotic status including platelet reactivity and spontaneous thrombolytic activity of 30 healthy young males (mean, 21.1 +/- 0.4 years) and 34 elderly males (64.5 +/- 1.1 years). The occlusion time (OT) and the lysis time (LT) were measured from a single native blood sample. The OT is an index of platelet activation and subsequent occlusive thrombus formation by high shear stress, while the LT is an index of the resumption of blood flow due to thrombolysis. The LTs in the elderly group were significantly longer than in the young group (P < 0.001). The LTs of elderly smokers were significantly longer than those of non-smokers (P < 0.001). Exercise did not affect the LT significantly. Platelet reactivity to shear stress (OT) was not affected either by aging, smoking or exercise habits. Suppressed spontaneous thrombolytic activity in elderly males and smokers could be a mechanism of acute thrombotic events in these people.

Adolescent↗
PubMed2006

Risk of excessive bleeding associated with marginally low von Willebrand factor and mild platelet dysfunction.

BACKGROUND: Bleeding symptoms are so commonly reported that it is not known whether they associate causally or coincidentally with mild but measurable primary hemostatic defects. OBJECTIVES/PATIENTS/METHODS: In order to evaluate if the mild primary hemostatic defects are truly causative of increased bleeding symptoms, we surveyed a population of healthy teenagers for bleeding symptoms. Using a case-control approach, we then estimated the risk of excessive bleeding associated with low von Willebrand factor (defined as VWF below the 5th percentile of a normal reference population), and with mild platelet dysfunction [PD, defined as concurrent reduced platelet aggregation responses to two agonists (adenosine diphosphate and epinephrine)]. RESULTS: Excessive bleeding was present in 63 out of 809 teenagers (7.8%). Among the 49 cases who were tested for VWF, low values by three measures were more commonly present than in 166 controls, specifically, ristocetin cofactor (RCo) activity [20.4% vs. 5.4%, odds ratio (OR) 4.5], collagen binding (14.3% vs. 4.2%, OR 3.8), and antigen level (20.4% vs. 6.0%, OR 4.0). The low RCo values ranged from 35 to 45 U dL(-1) except for a single case with 26 U dL(-1). Of the 47 teenagers with excessive bleeding who underwent platelet aggregation studies, reduced responses were more common than in controls (12.8% vs. 4.4%, OR 3.2). Twenty-nine per cent of cases with excessive bleeding had either low RCo or PD. CONCLUSION: Almost one in three teenagers who report excessive bleeding is likely to have a measurable hemostatic disturbance manifested either by marginally low VWF (by three measures) or by mild PD.

Adolescent↗
PubMed2005

Retention test Homburg to monitor the adhesive properties of von Willebrand factor after substitution or desmopressin therapy.

To diagnose von Willebrand disease (vWD) and to monitor drug efficacy, several tests have been established that are not, however, focused on the platelet adhesion properties of von Willebrand factor (vWF). The new platelet retention test Homburg (RTH) is characterized by a nonthrombogenic filter that retains platelets from blood when it is pressed through this filter. It was the aim of this study to examine the capability of this test to monitor the adhesive properties of vWF after its substitution in vWD or its release by desmopressin infusion. The RTH demonstrated a striking sensitivity for vWF after its release from endogenous storage sites or its supplementation in vivo as well as in vitro, whereas it did not detect an inhibition of platelet aggregability due to aspirin. Desmopressin infusions led to an immediate and highly significant increase of RTH platelet retention, followed by a gradual decline to initial values during the next 4 hours. The transfusion of a vWF concentrate also resulted in RTH data that demonstrated different kinetics than established parameters such as vWF:antigen, vWF:RiCoF, or the PFA-100 in vitro bleeding analysis. Additional in vitro experiments confirmed the correlation of RTH values with vWF concentrations. In conclusion, the RTH may be efficient to complement presently used measures to monitor vWD therapy with desmopressin or vWF concentrates.

Aspirin↗
PubMed2006

Pathophysiological processes underlying emotional triggering of acute cardiac events.

Acute negative emotional states may act as triggers of acute coronary syndrome (ACS), but the biological mechanisms involved are not known. Heightened platelet activation and hemodynamic shear stress provoked by acute stress may contribute. Here we investigated whether patients whose ACS had been preceded by acute anger, stress, or depression would show heightened hemodynamic and platelet activation in response to psychophysiological stress testing. We studied 34 male patients an average of 15 months after they had survived a documented ACS. According to an interview conducted within 5 days of hospital admission, 14 men had experienced acute negative emotion in the 2 h before symptom onset, and 20 men had not experienced any negative emotion. Hemodynamic variables and platelet activation were monitored during performance of challenging color-word interference and public speaking tasks and over a 2-h poststress recovery period. The emotion trigger group showed significantly greater increases in monocyte-platelet, leukocyte-platelet, and neutrophil-platelet aggregate responses to stress than the nontrigger group, after adjusting for age, body mass, smoking status, and medication. Monocyte-platelet aggregates remained elevated for 30 min after stress in the emotion trigger group. The emotion trigger group also showed poststress delayed recovery of systolic pressure and cardiac output compared with the nontrigger group. These results suggest that some patients with coronary artery disease may be particularly susceptible to emotional triggering of ACS because of heightened platelet activation in response to psychological stress, coupled with impaired hemodynamic poststress recovery.

Acute Disease↗
PubMed1996

An autosomal dominant, qualitative platelet disorder associated with multimerin deficiency, abnormalities in platelet factor V, thrombospondin, von Willebrand factor, and fibrinogen and an epinephrine aggregation defect.

Multimerin is a massive soluble, multimeric protein found in platelets and endothelial cells. Recent studies identified multimerin as a specific coagulation factor V binding protein, complexed with platelet, but not plasma, factor V. These findings led us to investigate individuals with inherited factor V deficiencies for possible multimerin abnormalities. Platelet proteins were evaluated using immunoassays, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, immunoblotting, immunoprecipitation, and direct binding studies. Patients with factor V Quebec, a disorder with abnormal platelet factor V, had a quantitative deficiency in multimerin (n = 11 tested; mean, 12.5%; range, 5% to 27% of the normal pool; normal range, 45% to 214%) with a normal multimer pattern. Quantitative and qualitative abnormalities were detected in their platelet factor V. An unrelated patient who was deficient in platelet and plasma factor V had normal platelet multimerin. The levels of platelet beta-thromboglobulin, von Willebrand factor, thrombospondin, and fibrinogen antigen were normal in the factor V Quebec patients. However, proteins with abnormal mobility were detected in their platelet lysate and releasate, and their platelet thrombospondin, von Willebrand factor, and fibrinogen showed evidence of proteolytic degradation. Platelet counts of the factor V Quebec patients ranged from mildly thrombocytopenic to low normal (mean, 159 x 10(9)/L; range, 104 to 198 x 10(9)/L). In addition, their platelets failed to aggregate in response to 6 to 10 micromol/L epinephrine despite normal numbers of platelet alpha 2-adrenergic receptors. These data indicate that patients with factor V Quebec have an inherited bleeding disorder distinct from other platelet disorders and associated with multiple abnormalities, including multimerin deficiency, abnormal platelet factor V, thrombospondin, von Willebrand factor, and fibrinogen, and an epinephrine aggregation defect.

Afibrinogenemia↗
PubMed1989

A comparative study of variables affecting the bleeding time using two disposable devices.

A number of variables affect the result of the bleeding time, the most frequently used test assessing primary hemostasis. Although the test is now usually performed with one of several commercially available disposable devices, most previous studies of the bleeding time have evaluated only the original template device described nearly 20 years ago. Therefore, we compared two commonly used bleeding time devices (Surgicutt and Simplate) with regard to multiple variables affecting the test in 40 hematologically normal young adults. Bleeding time was performed by the modified Ivy method according to the manufacturers' instructions in both horizontal (transverse) and vertical directions, before and two hours after a test dose of 650 mg of aspirin was administered. With both horizontal and vertical incisions, Simplate bleeding time values were greater than with the Surgicutt device (P = 0.0025). Bleeding time in the horizontal direction was greater than vertical with both devices (P = 0.0001). Values in males and females were not significantly different. Aspirin sensitivity, the difference between preaspirin and postaspirin values, was greatest with the use of the Surgicutt device in the horizontal position (mean postaspirin value 8.0 minutes). Both devices produced a reproducible uniform incision, caused minimal discomfort, and resulted in little or no scarring. The authors conclude that the results with Surgicutt and Simplate devices were comparable in many respects but that a horizontal Surgicutt bleeding time might be most sensitive in detecting disorders of primary hemostasis. Comparative studies of different bleeding time devices in normal subjects are necessary in order to accurately assess their clinical utility.

Adult↗
PubMed1993

The effect of acidified glucose nutrient solution on preservation of platelet concentrate.

The preservation effect of a new platelet solution--acidified glucose nutrient solution (AGN)--was tested by adding AGN to pooled platelet rich plasma (PRP) prior to preparation of platelet concentrates (PC). Each PRP unit was prepared from a unit of whole blood and four PRP of the same blood group were pooled in 400 ml volume PVC bags. Equal aliquots of each pooled PRP were made prior to preparation of PC. AGN was added to one aliquot and nothing was added to the control aliquot. Equal volume and concentration PC were then prepared and the PC were further aliquoted for storage at 22 degrees C. After five days, the parameters of platelet count, pH, aggregability and hypotonic shock response (HSR) for PC preserved in AGN plasma were better than those of the controls preserved in normal ACD plasma. The aggregability and HSR of AGN platelet concentrates recovered to baseline after two h of incubation with fresh plasma. The results of electron microscopy show that platelets preserved in AGN have less changes in morphology. The results of our work suggest that the preservation effect of AGN on PC is similar to the effect of using second generation containers or preparation of platelets from thrombocytapheresis.

Blood Platelets↗