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PubMed1986

[Methods of studying platelet function. Biological markers of the activation of human platelets in vivo and in vitro].

Platelets play a key role in hemostasis, thrombosis, atherosclerosis and their pathological consequences. It is possible to follow platelet activation in vivo by measuring bleeding time, platelet count, existence of circulating platelet aggregates or platelet survival and sequestration. In vitro tests include measurement of platelet adhesion, aggregation alpha, and dense granule secretion. It is also possible to follow biochemical events linked to platelet activation such as prostaglandin metabolism, Ca2+ levels or platelet membrane modifications (receptors, glycoproteins, coagulant activities, antigens). Some of these markers of platelet activation are modified in diseases (thrombotic events, hyperlipoproteinemia) and the use of artificial surfaces. It is not always possible to know if the modifications are the cause or the consequence of the pathological event. Unfortunately, some results are questionable because of methodological procedures. Some of these tests have been used to follow the involvement of platelets in a pathological event or to evaluate a prethrombotic state in a patient. It is not yet possible to identify directly, or by the mean of a marker of platelet activation, a patient who is likely to experience a thrombotic episode.

Blood Platelets↗
PubMed2001

Potentiation of ibudilast inhibition of platelet aggregation in the presence of endothelial cells.

Although communications between platelets and endothelial cells or other blood cells are important in in vivo thrombus formation, laboratory platelet function tests are usually performed in isolation from these surrounding cells. In this study, we evaluated the effect of an antiplatelet drug, ibudilast (3-isobutyryl-2-isopropylpyrazolo[1,5-a]pyridine), on platelet aggregation in the presence and absence of human umbilical vein endothelial cells (HUVECs) and with the use of platelet-rich plasma (PRP) or whole blood as platelet samples. Stimulation-dependent platelet aggregation was weakened in the presence of HUVECs, which was especially prominent when the thrombin receptor-activating peptide SFLL (compared with ADP and epinephrine) was used as an aggregating agent. Ibudilast hardly affected SFLL-induced platelet aggregation (in PRP), while this antiplatelet agent was found to clearly inhibit this SFLL-induced response in a concentration-dependent manner, in the presence of HUVECs. Ibudilast tended to inhibit ADP- or epinephrine-induced platelet aggregation in the presence of HUVECs, but the effects were not statistically significant. Enhanced inhibition by ibudilast of SFLL-induced platelet aggregation (in the presence of HUVECs) was reproduced with the use of whole blood samples when a screen filtration pressure method was employed. It is suggested that the platelet aggregation studies in the presence of endothelial cells and/or other blood cells provide us with valuable information on platelet reactivity in vivo and improvement of antiplatelet therapy.

Blood Platelets↗
PubMed1975

The effect of noradrenalin infusion on plasma and platelet lipids and platelet function in man.

Noradrenalin was given as an intravenous infusion in a dosage of 0.1 mu-g/kg/h over a period of 30 minutes to 5 healthy male subjects. Blood samples were collected before, at the end of and 24 hours after the infusion. A significant increase in the number of circulating platelets and a marked increase of plasma FFA, reflecting an increase of all the main components of the FFA fraction were observed. No significant changes were observed in the similar lipid fraction in platelets and except for a moderate increase in platelet factor 3 activity, no significant changes in other platelet function tests were present.

Adult↗
PubMed2002

Surface markers of platelet function in idiopathic nephrotic syndrome in children.

The objective of the study was to investigate platelet activation markers in whole blood in idiopathic nephrotic syndrome (INS) in children. The study group consisted of 34 children with 45 relapses of INS, 35 children in long-term remission of INS, and 26 healthy controls. Using flow cytometry we measured the percentage of platelet microparticles, platelet-platelet aggregates, and surface expression of CD62P (P-selectin) and CD42b (a component of von Willebrand factor receptor). We found an increased percentage of microparticles and platelet-platelet aggregates, decreased expression of CD42b in the first 2 weeks of INS relapse. CD62P expression was elevated only at the onset of INS relapse when compared with the long-term remission group and healthy subjects. Children in long-term INS remission did not differ from healthy controls. There was no significant correlation between platelet activation markers and selected biochemical factors of blood in children with INS. Activation of the coagulation cascade was confirmed by an elevated serum concentration of F1+2 prothrombin fragment during follow-up. These findings suggest that platelets may contribute independently to the prothrombotic state in the early stages of INS, but their role in triggering relapses remains to be investigated.

Adolescent↗
PubMed1977

Platelet function.

Basic knowledge regarding platelet physiology has been reviewed and related to clinical situations where platelet function is critically important. Platelet function tests such as aggregation and survival studies, which are research tools now, may soon be available to aid in the diagnosis and management of clinical bleeding problems. A growing understanding of drug-platelet interactions is allowing manipulation of platelets and the clotting system to improve the proganoses for patients who have thromboembolic diseases. Advances in platelet storage and transfusion techniques can save patients who previously might have bled to death. Proper application of the new developments in cardiopulmonary bypass and hemodilution, with attention to platelet and coagulation factor preservation, will contribute to securing hemostasis and conserving blood products.

Blood Coagulation Factors↗
PubMed1983

Thrombocytopenic purpura with giant platelets and ultrastructural platelet defects.

The case of a patient with thrombocytopenia and giant platelets is presented. Platelet function tests including bleeding time, aggregation, availability of PF3, and serotonin uptake and release were abnormal. A bone marrow aspirate showed megakaryocytes that while not increased in number, were young in appearance. Electron microscopy of platelets revealed a dilated surface-connecting canalicular system and a prominent membrane complex. No similar findings were encountered among the patient's relatives. The various diagnostic possibilities in this patient are discussed.

Adenosine Diphosphate↗
PubMed2002

Reductions in platelet contractile force correlate with duration of cardiopulmonary bypass and blood loss in patients undergoing cardiac surgery.

Blood loss secondary to platelet dysfunction is known to be increased when the duration of cardiopulmonary bypass (CPB) is prolonged. The ability to correlate alterations in platelet function with the duration of bypass and early postoperative blood loss, however, has remained elusive. Platelet contractile force, a novel measure of platelet-mediated clot retraction, is known to be reduced following cardiac surgery and blockade of platelet adhesion receptors. The aim of this study was to determine if alterations in platelet contractile force (measured using whole blood) correlated with the duration of CPB and early postoperative blood loss. Thirty patients were entered into a study designed to measure platelet function before, during, and after CPB. Platelet aggregometry and surface expression of CD42b and CD61 were also measured (using whole blood) in a subset of subjects (n=10) to further characterize the intrinsic structural and functional defects induced by CPB. Reductions in platelet contractile force had a significant correlation with duration of CPB (r=0.564; P=0.002) and early blood loss (r=0.545; P=0.003). Although decreases in platelet contractile force and aggregation both correlated with CPB time in the smaller subset of patients tested, only platelet contractile force correlated with decreases in CD42b, CD61 and blood loss. The results of this study suggest that prolongation of CPB is related to increasing degrees of platelet dysfunction and that reductions in platelet contractile force are related to decreases in platelet adhesion receptors and early postoperative blood loss.

Aged↗
PubMed1985

7-Bromo-1,5-dihydro-3,6-dimethylimidazo[2,1-b]quinazolin-2(3H)- one (Ro 15-2041), a potent antithrombotic agent that selectively inhibits platelet cyclic AMP-phosphodiesterase.

This study with the new analog Ro 15-2041 (7-bromo-1,5-dihydro-3,6-dimethylimidazo[2,1-b]quinazolin-2(3H)-on e) confirms and substantially extends the activity spectrum of imidazoquinazolinones as potent platelet function inhibitors. Ro 15-2041 inhibited platelet aggregation induced by all common platelet agonists in platelet-rich plasma obtained from various species including man (IC50 = 1-3 microM). The compound potentiated platelet inhibition by prostacyclin, the prostacyclin-induced increase of intraplatelet cyclic (c) AMP levels and inhibited the collagen-induced release of serotonin and beta-thromboglobulin. Ro 15-2041 reduced the increase and accelerated the normalization of cytosolic free Ca++ in thrombin-stimulated human platelets. Ro 15-2041 is a potent (IC50 = 70 nM) and selective inhibitor of platelet cAMP-phosphodiesterase activity. Whereas Ro 15-2041 caused complete inhibition of cAMP-phosphodiesterase activity in human platelet supernatants, breakdown of cAMP in cardiac homogenates was depressed to maximally 50%. In human brain and rabbit uterus Ro 15-2041 was at least 1000 times less potent. By comparison, papaverine fully inhibited phosphodiesterase activity in all four tissues with similar IC50 values of about 5 microM. Furthermore, Ro 15-2041 selectively inhibited cAMP-phosphodiesterase activity of a bovine calmodulin-independent but not of a calmodulin-dependent enzyme preparation. The compound exhibited significant p.o. activity in various ex vivo and in vivo platelet function tests.(ABSTRACT TRUNCATED AT 250 WORDS)

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1988

Diminished platelet residence time on active human atherosclerotic lesions in-vivo--evidence for an optimal dose of aspirin?

Although aspirin is an old drug, its optimal dose for the treatment of human atherosclerosis has not been finally proven. Various in-vitro and ex-vivo platelet function tests revealed a dose range from 1 to 3000 mg as being optimal. It was thus the goal to examine its in-vivo efficacy in human suffering from peripheral vascular disease in 7 different doses ranging from 1 mg to 1000 mg a day. All these patients have been treated for 3 months. Platelet half-life and platelet uptake ratio show an in part significant improvement being most pronounced at the daily doses of 20 and 1000 mg respectively. No change occurs in the placebo treated controls. These findings indicate, that 20 or 1000 mg aspirin taken daily per os, are superior to the other doses examined concerning the in-vivo platelet function (as measured by platelet half-life) and rendering the arterial surface less thrombogenic (as reflected by platelet uptake ratio-measurements).

Administration, Oral↗
PubMed2006

Escitalopram, but not its major metabolites, exhibits antiplatelet activity in humans.

BACKGROUND: Clinical depression has been identified as an independent risk factor for increased mortality during follow-up in patients suffered from acute coronary events, whereas increased platelet activity has been proposed as one of the mechanisms for this association. Some evidence suggests that selective serotonin reuptake inhibitors and/or their metabolites exhibit potent antiplatelet properties. METHODS: We assessed the in vitro effects of preincubation with escalating (50-200 nmol/L) concentrations of escitalopram (ESC) S-desmethyl-citalopram (S-DCT), and S-di-desmethyl-citalopram, (S-DCT) on platelet aggregation through the expression of major surface receptors using flow cytometry and quantitatively using platelet function analyzers in 20 healthy volunteers. RESULTS: Pretreatment of blood samples with ESC with ESC resulted in a significant inhibition of platelet aggregation induced by ADP (P = 0.0001) and by collagen with the highest dose (P = 0.001). Surface platelet expressions of glycoprotein Ib (CD42) (P = 0.04), lysosome associated membrane protein-3 (CD63) (P = 0.02), and GP37 (CD165) (P = 0.03) was decreased in the ESC-pretreated samples. Closure time by the Platelet Function Analyzer-100 analyzer was prolonged for the 200 nmol/L dose (P = 0.02), indicating platelet inhibition under high shear conditions. Two major metabolites of ESC, namely S-DCT and S-DDCT, did not affect platelet activity. CONCLUSION: Escitalopram, but not its metabolites, exhibited selective inhibition of human platelet properties. The direct antiplatelet effect of ESC requires further prospective or ex vivo testing to determine the possible clinical advantage of this finding.

Adult↗
PubMed1977

Postoperative platelet function in patients on small subcutaneous doses of heparin.

Several platelet function tests were performed on 31 patients undergoing major operations, who recieved prophylactically small subcutaneous doses of heparin. A group of 15 similar patients without heparin served as controls. It was found that postoperatively in both groups (a) the platelet retention in glass bead column was significantly increased (p less than 0.001), (b) the platelet aggregation by ADP 1 micronM was slightly increased, (c) the collagen-induced aggregation, ADP release and the bleeding time remained unchanged and (d) the platelet counts decreased in the first 2 postoperative days and increased thereafter. There was no difference between patients on heparin and controls.

Adenosine Diphosphate↗
PubMed1975

[Coagulation tests in von Willebrand's disease(author's transl)].

The diagnosis of von Willebrand's disease can be made by a selected series of easily performed clotting tests. A STudy of 36 patients with the disease (all but one with a mild form) revealed a significantly increased reaction time in the thrombelastogram from 210 plus or minus 33 percent to 270 plus or minus 69 percent (P less than 0.001), and of the partial thromboplastin time from 43 plus or minus 3s to 54 plus or minus 9s (P less than 0.001 than 0.001). Factor VIII activity was corresponding significantly reduced from normal (127 plus or minus 51 percent) to 51 plus or minus 12 percent (P less than 0.001). Other plasma factors and platelet counts were within normal limits. A platelet defect was indicated by an abnormal change in the speed of clot formation (k-time) from 162 plus or minus 39 percent to 341 plus or minus 121 percent (P less than 0.001), maximal thrombelasticity from 121 plus or minus 16 percent to 75 plus or minus 22 percent (P less than 0.001), and marked reduction in platelet-factor 3 liberation from 122 plus or minus 59 percent to 23 plus or minus 16 percent (P less than 0.001). An increase in bleeding time, from 162 plus or minus 41s to 204 plus or minus 128s (P less than 0.05), was not always present. Recently introduced immunological methods for determining factor VIII and factor VIII-associated protein, as well as special platelet-function tests, give further information on the pathogenesis of the bleeding disease, but their complexity restricts them to special laboratories.

Blood Coagulation Factors↗
PubMed2003

Effects of PEG-hirudin in clotting parameters and platelet function and its interaction with aspirin in healthy volunteers.

The purpose of this study was to investigate the pharmacodynamics of PEG-Hirudin and its potential interactions with acetylsalicylic acid (ASA 325 mg once daily from days 1-3). In a randomized, 2-way cross-over trial, 6 healthy volunteers received PEG-Hirudin (i.v. bolus of 0.2 mg/kg + 0.02 mg/kg/h for 24 hours) and placebo (i.v. bolus + 24-hour infusion). In a further randomized, 3-way cross-over trial another 9 healthy volunteers received ASA (325 mg) or oral placebo from days 1 to 3 and PEG-Hirudin (0.2 mg/kg + 0.02 mg/kg/h for 24 h) or i.v. placebo on day 3. Assessments included bleeding time (BT), collagen (1 microgram ml(-1))-induced platelet aggregation (CIPA), platelet adhesion, ecarin clotting time (ECT), activated clotting time (ACT), plasma anti-factor IIa activity (aIIa), and activated partial thromboplastin time (aPTT). Ten minutes after the PEG-Hirudin injection/starting the infusion, mean plasma concentration was 3.1 microgram/mL and aPTT, ECT, and ACT were prolonged up to 80, 309, and 233 seconds, respectively. During the last 8 hours of the 24-hour infusion mean PEG-Hirudin plasma concentration was 1.3 microgram/mL. In the interaction study, ASA significantly inhibited CIPA. At 6 hours after administration, on day 3 mean BT was 6.5 minutes after PEG-Hirudin alone, 18.2 minutes after ASA alone, and 32.9 minutes after combined administration of ASA and PEG-Hirudin. PEG-Hirudin (0.2 mg/kg + 0.02 mg/kg/h for 24 hours) administered alone or together with 325 mg ASA proved to be safe in healthy volunteers. Combined use of PEG-Hirudin and ASA significantly increased the mean bleeding time compared to ASA or PEG-Hirudin monodrug administration. None of the clotting parameters or platelet function tests correlated with the prolongation of the bleeding time.

Aspirin↗
PubMedDate not supplied

Effects of drugs on platelet function.

Numerous drugs and chemicals affect the function of human blood platelets. The mechanism of action of some medications is partly understood. Aspirin is the most frequently involved drug. It appears to interfere with the platelet release reaction by acetylation of a platelet membrane protein which may be involved in the synthesis of prostaglandins. Other anti-inflammatory drugs, including indomethacin, phenylbutazone, ibuprophen (Motrin) and clonixin, also interfere with the release reaction but have a shorter acting course than aspirin. Some drugs stimulate adenylcyclase (gliclazide) or block phosphodiesterase, (dipyridamole, caffeine) both of which actions lead to an increase in adenosine cyclic 3':5' monophosphate (cAMP) and decrease aggregation by adenosine diphosphate (ADP). These interactions should be known to clinical scientists since patients using these medicaments may manifest abnormal platelet function tests in the laboratory and mild hemorrhagic syndromes in the clinic.

Adenosine Diphosphate↗
PubMedDate not supplied

Decreased platelet function in Cavalier King Charles Spaniels with mitral valve regurgitation.

With aggregometry, increased platelet activity has been reported in Cavalier King Charles Spaniels (CKCS) without mitral regurgitation (MR). In contrast, dogs with MR have been found to have decreased platelet activity. The purpose of this study was to test an easy bedside test of platelet function (the Platelet Function Analyzer [PFA-100]) to see if it could detect an increase in platelet activity in CKCS without MR and a decrease in platelet activity in CKCS with MR. This study included 101 clinically healthy dogs > 1 year of age: 15 control dogs of different breeds and 86 CKCS. None of the dogs received medication or had a history of bleeding. The PFA-100 evaluates platelet function in anticoagulated whole blood under high shear stress. Results are given as closure times (CT): the time it takes before a platelet plug occludes a hole in a membrane coated by agonists. The CT with collagen and adenosine-diphosphate as agonists was similar in control dogs (median 62 seconds; interquartile interval 55-66 seconds) and CKCS with no or minimal MR (55; 52-64 seconds). The CT was higher in CKCS with mild MR (regurgitant jet occupying 15-50% of the left atrial area) (75; 60-84 seconds; P = .0007) and in CKCS with moderate to severe MR (jet > 50%) (87: 66-102 seconds; P < .0001). CKCS with mild, moderate, and severe, clinically inapparent MR have decreased platelet function. The previous finding of increased platelet reactivity in nonthrombocytopenic CKCS without MR could not be reproduced with the PFA-100 device.

Animals↗