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 271 records · Page 15Linked to original sources
PubMed1999

Performance of the platelet function analyser PFA-100 in testing abnormalities of primary haemostasis.

The PFA-100 device is a new instrument for the in-vitro testing of platelet function. Primary haemostasis is stimulated by recording the closure time taken for platelets to seal a 150 microm aperture in the centre of a membrane coated with collagen and either epinephrine or ADP. Patients with type 3 von Willebrand's disease (n = 4) all had infinitely prolonged closure times (> 200 s) with both types of cartridge. A patient with afibrinogenemia exhibited only slightly prolonged closure times of 111 and 166 s for the ADP and epinephrine membranes, respectively. Patients with Glanzmann's thrombasthenia (n = 6) and Bernard Soulier syndrome (n = 2) had grossly prolonged closure times (> 200 s) with both types of cartridges. These results confirmed that the PFA-100 system was highly dependent on normal von Willebrand factor, glycoprotein Ib and glycoprotein IIb/IIIa levels but not on plasma fibrinogen. Patients with storage pool disease (n = 6) and Hermansky Pudlak syndrome (n = 7) had prolonged closure times with the epinephrine cartridge. There was no evidence of enhanced platelet function in patients with antiphospholipid syndrome, in sickle-cell disease or thalassemia. However, ingestion of aspirin resulted in a near consistent and significant prolongation of the closure time for the epinephrine cartridge but not for the ADP cartridge in both normal subjects and patients. The test offers a reliable, reproducible, rapid and simple means of assessing high-shear platelet function in vitro.

Blood Platelets↗
PubMed2005

Testing various herbs for antithrombotic effect.

OBJECTIVE: Prevention of arterial thrombotic diseases has high priority in developed countries. Because people who eat inappropriate food are prone to thrombotic events, regular intake of an antithrombotic diet may offer a convenient and effective way of prevention. The aim of the present study was to find herbs that have antithrombotic effects. METHODS: Herbs were crushed and centrifuged and the juice obtained was filtered. The effect of filtrate on platelet-rich thrombus formation was assessed by a shear-induced in vitro platelet function test (hemostatometry). Filtrates showing significant antithrombotic activity were further assessed by using a laser-induced in vivo thrombosis test in mice. The effect of orally administered herb filtrates on flow-mediated vasodilation was also measured. RESULTS: Common thyme and rosemary showed significant antithrombotic activity in vitro and in vivo. Neither herb affected flow-mediated vasodilation. CONCLUSION: Some herbs possess antithrombotic effects in experimental models of thrombosis. The mechanism of the antithrombotic effect of common thyme and rosemary may involve a direct inhibitory effect on platelets.

Animals↗
PubMed1985

[Platelet function after the single administration of buflomedil].

Earlier investigations have demonstrated that buflomedil, a substance which is successful in the clinical treatment of peripheral vascular disease, exerts an inhibitory effect on ADP-induced aggregation ex vivo and in vitro. In the presented study the effect of buflomedil on platelets is investigated. Clinically widely used platelet function tests were performed after a single oral dose of buflomedil (300 mg) to healthy volunteers. Again, an ex vivo inhibition of ADP-induced aggregation was confirmed. None of the other parameters examined was influenced by the administered drug, such as plasma thromboxane B2, the platelet proteins, the platelet sensitivity to antiaggregatory prostaglandins and the prostacyclin synthesis stimulating plasma factor.

Adult↗
PubMed2006

Comparison of VASP-phosphorylation assay to light-transmission aggregometry in assessing inhibition of the platelet ADP P2Y12 receptor.

There is need to improve platelet function testing to monitor the response to antiplatelet drugs. We compared flow-cytometric analysis of intraplatelet vasodilator-stimulated phosphoprotein phosphorylation (VASP-P) to light-transmission aggregometry for the detection of drug-induced in-vitro inhibition of the platelet P2Y12 ADP receptor on 22 healthy subjects (10 males, 12 females, 28.5 +/- 6.6 years). The platelet reactivity index (PRI) of VASP was calculated both from mean fluorescence intensity (MFI) and percent of fluorescence-positive platelets in the presence of PGE1 with or without ADP (10 microM). Platelet aggregation was induced by ADP (1.25, 2.5 and 5 microM). Cangrelor, a competitive inhibitor of the P2Y12 receptor, preincubated 5 minutes, induced a concentration-dependent inhibition of platelet ADP-receptor function in both tests. Indeed PRI (%) based on either MFI or percent platelets gated were highly correlated with each other (r = 0.97, p %lt; 0.0001) and with aggregation induced by ADP. The IC50 of cangrelor against each of the three ADP concentrations used in aggregometry increased from 5.8 +/- 3.4 nM to 23.1 +/- 4.0 nM and to 98 +/- 25 nM, respectively. The IC50 of cangrelor based on VASP-P was within the same range (25.5 +/- 7.7 nM). No correlation was observed between IC50 values of cangrelor and ADP concentrations giving 50% effect (EC50) in the absence of the drug. However, at 10 nM cangrelor seven subjects could be identified by the VASP-P assay as " low responders " to the drug (PRI > 50%), and six of them also had an aggregation response to 5 micro M ADP > 50%. These six subjects showed the lowest ADP EC50 values in the absence of the drug, possibly reflecting high sensitivity of their platelet P2Y12 receptors to ADP. In conclusion, both the VASP-P assay and light-transmission aggregometry detect in a comparable way in-vitro pharmacological inhibition of the platelet P2Y12 ADP receptor and its individual variability.

Adenosine Diphosphate↗
PubMed2002

Comparison between nasal and intravenous desmopressin for the treatment of aminosalicylic acid-induced platelet dysfunction.

BACKGROUND AND OBJECTIVE: The study was conducted to compare the standard intravenous route with the intranasal route of desmopressin application and to establish the best time for initiating treatment with desmopressin with the use of the Born test and the PFA 100-Analyzer for monitoring the therapeutic effect. METHODS: Thirty healthy volunteers (ASA I) with no known bleeding disorder were randomly assigned to an intravenous or an intranasal group in a cross-over design fashion. After obtaining baseline values, the volunteers were given 500 mg aminosalicylic acid for 3 days. On day 4, platelet function tests were performed and desmopressin (0.3 microg kg(-1) body weight) was administered either intravenously or intranasally. Born tests (aggregation after stimulation with epinephrine and collagen) were conducted at 30 and 240 min, and PFA 100 bleeding time measurements were conducted at 30, 120 and 240 min after desmopressin administration. Wilcoxon signed rank sum tests or non-parametric ANOVA for repeated measures were used for statistical evaluation. RESULTS: All volunteers showed a marked decreased platelet function in the Born test (especially if stimulation with epinephrine was used) and an increased PFA 100 bleeding time after treatment with aminosalicylic acid. Platelet function was improved by intravenous as well as intranasal application of desmopressin (P < 0.001) after 30 min. The effect diminished after 4 h in both groups. CONCLUSIONS: Intravenous as well as intranasal desmopressin improved platelet function in healthy volunteers with aminosalicylic acid-induced platelet dysfunction at least 30 min after application. The effect lasts up to 4 h.

Administration, Intranasal↗
PubMed1989

Acquired platelet dysfunction with eosinophilia: review of seven adult cases.

Seven adults with acquired platelet dysfunction with eosinophilia presented with histories of spontaneous bruising and three also had moderate thrombocytopenia. Six patients had platelet function tests performed and all showed variable storage pool defects. When assayed, IgE concentrations were raised. Although only two patients had parasites isolated in their stools, all seven responded to antihelminth treatment. It is speculated that the IgE response to parasites mediates mast cell degranulation, which leads to in vivo platelet activation.

Adult↗
PubMed1982

Platelet function in rheumatoid arthritis.

Platelet function tests were evaluated in 20 patients with rheumatoid arthritis (RA), 9 of whom displayed thrombocytosis (greater than 400,000 platelets/microliter). Most patients had an enhanced sensitivity to collagen and epinephrine induced aggregation, as compared with a reference group. In contrast, malondialdehyde (MDA) production, an index of platelet arachidonic acid metabolism, was in the normal range for all the patients except 3, who were LE phenomenon positive. The hypersensitivity of platelets to aggregating stimuli was particularly marked in thrombocytotic patients, who also showed the most striking biochemical and clinical abnormality. These findings indicate the crucial role of platelets in the development and self-sustaining of RA.

Adult↗
PubMed1989

Platelet function during long-term treatment with ketanserin of claudicating patients with peripheral atherosclerosis. A multi-center, double-blind, placebo-controlled trial. The PACK Trial Group.

In a multi-center, double-blind, placebo-controlled trial in claudicating patients with peripheral atherosclerosis, the effects of 1 year of treatment with ketanserin (20 mg t.i.d. for 1 month, 40 mg t.i.d. thereafter; n = 63 patients) or placebo (n = 84 patients) on platelet function (aggregation in P.R.P. by 5-HT 5 x 10(-6) M, ADP 1 to 5 x 10(-6) M, collagen 2 micrograms/ml; platelet 5-HT content; plasma beta TG- and PF4-levels; serum TXB2) were analyzed. Before treatment, claudicating patients (n = 173) displayed an higher reactivity of platelets to 5-HT and signs of platelet activation/release in vivo (higher plasma beta TG-PF4, lower platelet 5-HT content and decreased platelet aggregation by ADP, collagen) in comparison with healthy controls (n = 50). After 1 year of treatment with ketanserin, but not with placebo, platelet aggregation induced by 5-HT (slope -41.1%) and platelet 5-HT content (-23.7%) were significantly reduced. PF4 and beta TG were significantly higher than their pre-medication values in the two trial groups. The other platelet function tests were not significantly modified by the treatment. Only the small subgroup of patients with initially elevated plasma beta TG levels (greater than 20 ng/ml) also scrutinized for hidden NSAID consumption or technical bias (exclusion of data with serum TXB2 less than or equal to 10000 pg/100 microliters and/or plasma PF4 greater than 10 ng/ml) had significantly lower plasma beta TG levels (-22.7%) than the pre-medication values after treatment with ketanserin, but not with placebo. The present study confirms that ketanserin affects some platelet functions, during long-term administration in claudicating patients with atherosclerosis.

Calcium↗
PubMed1985

Low haematocrit and prolonged bleeding time in uraemic patients: effect of red cell transfusions.

This study demonstrates that a low haematocrit is the main determining factor of the prolonged bleeding time often encountered in uraemic haemodialysed patients. Thirty-three patients submitted to regular haemodialysis and having a platelet count greater than 100 X 10(9)/l were investigated with the following tests: simplate bleeding time, blood cell count, platelet aggregation induced by ADP, collagen and sodium arachidonate, arachidonate induced MDA synthesis, tests for detection of an acquired storage pool disease, and factor VIII complex level. The results were compared to two other groups; one of uraemic patients not yet subjected to haemodialysis and another of healthy volunteers. The results were basically identical in the two groups of uraemic patients. The only consistent abnormality was a 30-35% reduction in the platelet MDA synthesis in comparison with control subjects. There was a negative correlation between the log bleeding time and the haematocrit (r = 0.78, P less than 0.01). Fourteen uraemic patients having a prolonged bleeding time were submitted to a red cell transfusion programme and were investigated a second time under identical conditions. There was no change in any of the platelet function tests or in the factor VIII complex level, but the bleeding time was normalized when the post-transfusion haematocrit was over 26% (nine patients). This study emphasizes the role of anaemia in the pathogenesis of the prolonged bleeding time in uraemia and suggests that red cell transfusion can be a long-term efficient therapeutic measure to stop bleeding in these patients.

Adolescent↗
PubMed1992

Contribution of perfusion techniques to the evaluation of the hemostatic effectiveness of platelet concentrates.

Perfusion systems allowing the morphometric analysis of platelet interactions with vessel subendothelium under flow conditions have been applied to evaluate the quality and function of stored platelets. Studies performed in vitro indicate that despite the existence of storage lesions, platelets in concentrates stored for up to 5 days retain their ability to interact with the subendothelium. Perfusion studies ex vivo with nonanticoagulated blood from anemic-thrombocytopenic patients have shown the critical hemorrheological role of red blood cells facilitating platelet interactions with subendothelium. Similar studies performed on severely thrombocytopenic patients who received transfusions of platelets stored at 4 degrees C indicate that incompletely viable platelets can contribute to primary hemostasis through procoagulant mechanisms. The latter results suggest that storage lesions which contribute to impairment of platelet function may result in enhancement of platelet procoagulant activities. Perfusion techniques have contributed to the evaluation of the hemostatic effectiveness of platelet concentrates. These techniques will provide a useful model to test the impact of new storage technologies on platelet hemostatic function.

Animals↗
PubMed2001

Influence of the genetic background on platelet function, microparticle and thrombin generation in the common laboratory mouse.

Genetic background has been shown to affect phenotype in transgenic mice with hemostatic defects. We present comparative data on various platelet function tests, as well as on microparticle and thrombin generation capacity in three mouse strains most commonly used in transgenic applications. Normal, inbred 129Sv (n = 24), C57BL/6 (n = 14) and BALB/c (n = 22) mice were used. BALB/c mice showed statistically significantly longer tail-bleeding times (158 +/- 42 s, P<0.02) than 129Sv (113 +/- 37) and C57BL/6 (122 +/- 29) and paradoxically increased velocity of platelet aggregation (P<0.01) with ADP, collagen, ionophore and thrombin. ATP-release did not differ between strains, it was weakest with ADP and strongest with thrombin. 129Sv platelets were less responsive to thrombin. Generation of platelet microparticles did not differ between strains either and could efficiently be inhibited by EDTA but not by aspirin or alprostadil. Two anti-GPIIIa monoclonal antibodies did not inhibit microparticles either, although they could block aggregation. Thrombin generation was equivalent in C57BL/6 and BALB/c, but slower in 129Sv. Interestingly, the reaction in all strains was immediate and different from the human model in that no lag-phase was seen after triggering. In summary these mouse strains show similar patterns of ex vivo platelet aggregation, bleeding times as well as microparticle and thrombin generation. Subtle differences were found, which should be taken into consideration when interpreting data from wild-type or transgenic models.

Animals↗
PubMed2003

A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease.

OBJECTIVES: This study was designed to determine if aspirin resistance is associated with clinical events. BACKGROUND: Aspirin resistance, defined by platelet function testing and presumed clinical unresponsiveness to aspirin, has been previously reported by our group and others. However, little information exists linking the laboratory documentation of aspirin resistance and long-term clinical events. METHODS: We prospectively enrolled 326 stable cardiovascular patients from 1997 to 1999 on aspirin (325 mg/day for > or =7 days) and no other antiplatelet agents. We tested for aspirin sensitivity by optical platelet aggregation using adenosine diphosphate (ADP) and arachidonic acid (AA). The primary outcome was the composite of death, myocardial infarction (MI), or cerebrovascular accident (CVA). Mean follow-up was 679 +/- 185 days. Aspirin resistance was defined as a mean aggregation of > or =70% with 10 microM ADP and > or =20% with 0.5 mg/ml AA. RESULTS: Of the patients studied, 17 (5.2%) were aspirin resistant and 309 (94.8%) were not aspirin resistant. During follow-up, aspirin resistance was associated with an increased risk of death, MI, or CVA compared with patients who were aspirin sensitive (24% vs. 10%, hazard ratio [HR] 3.12, 95% confidence interval [CI] 1.10 to 8.90, p = 0.03). Stratified multivariate analyses identified platelet count, age, heart failure, and aspirin resistance to be independently associated with major adverse long-term outcomes (HR for aspirin resistance 4.14, 95% CI 1.42 to 12.06, p = 0.009). CONCLUSIONS: This study demonstrates the natural history of aspirin resistance in a stable population, documenting a greater than threefold increase in the risk of major adverse events associated with aspirin resistance.

Adult↗
PubMed1978

Correction of the bleeding time in patients with storage pool deficiency by infusion of cryoprecipitate.

Five patients with Hermansky-Pudlak syndrome: storage pool deficiency, albinism and ceroid containing bone marrow macrophages and three patients with uncomplicated storage pool deficiency were treated with cryoprecipitate from 16 donors. Within 2 h of transfusion, bleeding times decreased towards a third of initial values. This effect lasted for at least 4 h but had disappeared after 24 h. Six of these eight patients were also treated with an equal volume of human albumin solution. Infusion of albumin had no effect on the bleeding times. The abnormal platelet function tests and biochemical abnormalities (decreased values of platelet total adenosine diphosphate (ADP), adenosine triphosphate (ATP(I) and serotonin) remained unchanged. On four occasions infusion of cryoprecipitate twice daily protected patients with Hermansky-Pudlak syndrome and storage pool deficiency from bleeding during surgery. The mechanism of action of cryoprecipitate in this clinical situation is obscure.

Adenosine Diphosphate↗
PubMed1976

Platelet hyperaggregability in idiopathic recurrent deep vein thrombosis.

Studies of platlet function were performed in 30 patients with idiopathic recurrent venous thrombosis. Evidence of platelet hyperactivity was found in 14 patients who exhibited spontaneous platelet aggregation and in 13 patients who had evidence of circulating platelet aggregates. No other differences in clinical characteristics or coagulation parameters could be elucidated between these two subgroups. In nine patients who had 51Cr-labeled platelet survival studies, there was a good correlation between the platelet hyperactivity and shortened platelet survival. Spontaneous platelet aggregation was inhibited both in vivo and in vitro by aspirin. In addition, the circulating platelet aggregates were normalized by combination treatment with aspirin and dipyridamole. The results indicate that the idiopathic recurrent venous thrombosis patient population could be differentiated by the platelet function tests into subgroup I, in which no platelet abnormality could be detected, and subgroup II, where platelet hyperaggregability was present. These results indicate that the role of platelets should be considered in the pathogenesis of recurrent venous thrombosis and therapy with agents which inhibit platelet aggregation may be beneficial in the patients with platelet hyperaggregability.

Adult↗
PubMed1995

Familial macrothrombocytopenia with unusually elongated mitochondria.

We report a familial case of macrothrombocytopenia without inclusion bodies in polymorphonuclear cells or any congenital abnormalities. The results of the hemostatic and platelet function tests were all normal except for the platelet retention rate. The number of megakaryocytes increased slightly and some were relatively small. Electron microscopic studies revealed a unique morphological abnormality of the platelets' mitochondria.

Adult↗
PubMed1988

[Calcium antagonists: anti-atherosclerotic effect by modification of the prostaglandin system].

The aim of the study was to investigate the influence of calcium blockers on the prostaglandin system of blood platelets and the vessel wall with respect to a possible beneficial effect on atherosclerosis. The influence of diltiazem, isradipine, nifedipine and verapamil was examined on ADP- and collagen-induced in vitro platelet aggregation, platelet malondialdehyde formation and other platelet function tests. All the calcium blockers investigated inhibited platelet activation in a dose-dependent manner, isradipine being the most effective. Malondialdehyde formation (measured photometrically) and thromboxane (TX) B2 production were decreased too. Vascular tissue PG12 formation was investigated in rat aortic rings (6-oxo-PGF1 alpha-RIA). PG12 formation was enhanced by all the calcium blockers investigated (p less than 0.01), isradipine again having the most pronounced effect. Platelet adenylate cyclase was stimulated by diltiazem only (RIA, HPLC). Ex vivo ADP-, collagen- and epinephrine-induced platelet aggregation and serum TX were studied 90 minutes after ingestion to diltiazem (60 mg), nifedipine (20 mg) and verapamil (40 mg). ADP- and epinephrine-induced platelet aggregation (19-36%) and serum TX were reduced significantly (p less than 0.01), but collagen-induced aggregation was not significantly affected. These results suggest a possibly beneficial effect of calcium blockers on atherosclerosis via the prostaglandin system.

Adult↗
PubMed1988

Platelet function and the bleeding time in progressive renal failure.

Bleeding time and platelet function tests were performed on 31 patients with progressive chronic renal failure (CRF) due to non-immunological (urological) causes, and compared with 22 healthy controls. Patients were classified as mild (plasma creatinine less than 300 mumol/l), moderate (300-600 mumol/l) or severe renal failure (greater than 600 mumol/l). Bleeding time was rarely prolonged in mild and moderate CRF and mean bleeding time significantly elevated only in severe CRF (p less than 0.005). Haematocrit was the only index which correlated with bleeding time (r = -0.40). Platelet counts, collagen stimulated thromboxane generation, and platelet aggregation responses to ADP, collagen and ristocetin were all either normal or increased in all three CRF groups, but thromboxane production in clotting blood was reduced. Plasma fibrinogen, C reactive protein and von Willebrand factor (vWF) were elevated in proportion to CRF. We found no evidence that defects in platelet aggregation or platelet interaction with vWF prolong the bleeding time in patients with progressive CRF.

Bleeding Time↗
PubMed1990

Effects of carvedilol on common carotid arterial flow, peripheral hemodynamics, and hemorheologic variables in hypertension.

The effects of a beta-blocker, carvedilol, on peripheral hemodynamics and hemorheologic parameters were evaluated in 11 geriatric patients with essential hypertension [3 men and 8 women aged 62-79 years (mean, 68.6 years)]. Carvedilol was given orally after breakfast at a dose of 10 or 20 mg daily for 8 weeks. Peripheral hemodynamics, the common carotid arterial flow, and hemorheologic parameters were determined twice prior to administration and after 4 and 8 weeks of carvedilol treatment. The common carotid arterial flow was determined using the pulsed Doppler method. Peripheral hemodynamics were assessed by venous occlusion plethysmography. The hemorheologic parameters assessed include erythrocyte aggregation, erythrocyte deformability, plasma viscosity, whole-blood hematocrit, and platelet function tests. Erythrocyte aggregation was measured using an Erythrocyte Aggregometer MA-1 (Myrenne, USA), taking a high shear rate of 600 s-1 and a low shear rate of 3 s-1 as the indices. Statistical comparisons of values before and after carvedilol administration were made using the paired Student's t-test. Systolic and diastolic blood pressure were decreased by carvedilol. The common carotid arterial flow was increased, and peripheral hemodynamics were improved by carvedilol. Erythrocyte aggregation (measured at both a high and a low shear rate) and plasma viscosity were decreased, erythrocyte deformability was increased, and levels of circulating platelet aggregates were also improved by carvedilol. This improvement of hemorheologic variables may contribute to prevention of the initiation and progression of thrombosis and atherosclerosis in geriatric patients with essential hypertension.

Adrenergic beta-Antagonists↗