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PubMed1981

Accuracy of low electronic platelet counts using platelet distribution curves.

At low platelet levels electronic counts are inaccurate because background counts are an increasingly important contribution to the total count. In this study the background contribution was selectively eliminated by coupling a multichannel particle size analyzer (Coulter Channelyzer II) to an electronic counter (Coulter ZBI). Platelet counts below 50 x 10(9)/l required an adjustment of the lower threshold in 11 of 15 specimens. Non-platelet counts averaged 18 percent of the platelet particle count with a maximum value of 50 percent. In contrast, platelet counts between 50 to 100 x 10(9)/l required only a minimum adjustment of the lower threshold and extraneous counts averaged only 2.7 percent of the platelet particle count. Phase platelet counts ranging from 4.0 x 10(9)/l to 115 x 10(9)/l were compared in ZBI-Channelyzer counts in 30 patients. The electronic counts showed good agreement with the reference method. Results were statistically analyzed using linear regression analysis and paired t tests. Technical errors involved in electronic and visual platelet counts are discussed.

Blood Platelets↗
PubMed1994

Blood platelets in experimental lung emphysema. Comparative analysis of the number and aggregation abilities of platelets in left and right ventricular blood of the heart.

Quantitative and morphological analyses (in SEM) of blood platelets collected from the left and right ventricles of the rat heart in the course of experimental lung emphysema were done. Platelet aggregation index was estimated, too. Emphysema was induced by a single intratracheal instillation of papain solution in a dose of 20 mg/kg b.w/1 ml PBS. The animals were sacrificed after 2 and 24 hours and 7, 14, 28 days later. Within 24 hours of the experiment a slight decrease was observed in the number of platelets in the blood collected from the left ventricle compared to the right one as well as to control animals. Also a reduction in platelet aggregation coefficient value was noted. However, in the later period of emphysema progression (after 7th day), a statistically significant increase was found in the number of blood platelets in the left ventricle. A relation was noted between quantitative changes of blood platelets and emphysema progression evaluated morphometrically. The ultrastructural examinations in SEM suggest the occurrence of platelet satellitosis in animals intratracheally injected with papain solution. The present results indicate the possibility of a significant contribution of blood platelets to the pathogenesis of experimental lung emphysema.

Animals↗
PubMed1993

Flow cytometric analysis of surface membrane proteins on activated platelets and platelet-derived microparticles from healthy and thrombasthenic individuals.

We used flow cytometry to investigate surface membrane protein expression by platelets and platelet-derived microparticles from normal individuals and a patient with Glanzmann's thrombasthenia. Microparticles were detected by both forward scatter and side scatter using FACScan. The binding of coagulation factors on microparticles was investigated by using monoclonal anti-Factor IX (IXa) and anti-Factor X (Xa) antibodies. Furthermore, the procoagulant activity of microparticles was measured with a chromogenic substrate (S-2222) using a microtiter enzyme-linked immunosorbent assay. Both types of platelets showed similar release of microparticles. Microparticles released from platelets after activation with the calcium ionophore A23187 did not bind factors IXa and Xa, but when purified factors Va and Xa were added to the incubation buffer, factor Xa binding increased markedly in both normal and thrombasthenic platelets. Both normal and thrombasthenic platelets showed a similar time-dependent release of microparticles when activated with A23187. However, the binding of an antibody to granule membrane protein-140 also increased time-dependently in normal microparticles, but was little increased in thrombasthenic microparticles. These findings suggest that glycoprotein IIb/IIIa does not participate in the expression of prothrombinase activity on the surface of activated platelets and microparticles, whereas this glycoprotein appears to have an important role in the movement of granule membrane protein-140 from platelets to microparticles.

Adult↗
PubMed1997

Ganglioside content of human platelets--differences in resting and activated platelets.

Gangliosides may play functional roles in platelet physiology, therefore this study has been designed to evaluate whether changes in ganglioside composition may occur as a consequence of platelet activation. The results obtained indicate that lactosylceramide and GM3 are the major glycosphingolipids of human platelets. The lipid-bound sialic acid (LBSA) content was 1.27 +/- 0.04 micrograms/mg of protein. Resting platelets did not express GD3; GD3 was synthesized upon platelet activation (24 +/- 8 ng/mg of protein). The stimulation of platelets with adenosine diphosphate showed the appearance of GD3 even in the absence of degranulation. Finally, incorporation of pyrene-labeled GM3 into platelet membranes, followed by stimulation with adenosine diphosphate, resulted in the appearance of a fluorescent band comigrating with GD3. The present studies indicate that sialytransferase activation may occur as an early event following platelet stimulation, leading to GD3 synthesis mainly from the GM3 pool.

Blood Platelets↗
PubMed1977

Intravascular aggregation and pulmonary sequestration of platelets during IgE-induced systemic anaphylaxis in the rabbit: abrogation of lethal anaphylactic shock by platelet depletion.

Significant alterations in the circulatory properties of platelets have been documented during IgE-induced systemic anaphylactic shock in the rabbit. Within 30 to 60 sec after i.v. antigen challenge, platelet aggregation occurs in both the venous and arterial circulations. The platelet aggregates then sequester in small blood vessels of various organs, particularly in the lung. The organ sequestration results in the development of a profound thrombocytopenia within 3 to 5 min after antigen challenge. Fifteen min later deaggregation of platelets occurs and the platelets return to the peripheral circulation within normal, prechallenge levels by 60 min. Additional experiments demonstrated that platelet depletion before antigen challenge abrogates the lethal effects and significantly reduces the pathophysiologic manifestations of IgE-induced systemic anaphylaxis. We conclude that the IgE-induced platelet alterations, probably induced by the intravascular release of basophil and perhaps mast cell-derived platelet-activating factor (PAF), play a major role in the pathogenesis of systemic anaphylaxis in the rabbit.

Anaphylaxis↗
PubMed1997

The effects of platelet inhibitors on platelet uptake and restenosis after femoral angioplasty.

OBJECTIVE: To investigate the effects of two platelet inhibitors, aspirin and iloprost, on platelet uptake and restenosis at the site of angioplasty in patients undergoing femoral or popliteal angioplasty. EXPERIMENTAL DESIGN: Prospective, open, randomised group comparison. SETTING: Two university hospitals. PATIENTS: 43 patients undergoing femoral or popliteal angioplasty were randomised. INTERVENTIONS: Patients received either aspirin (300 mg/day), iloprost (8 hours/day i.v. infusion) or no antiplatelet medication during angioplasty and on the subsequent two days. MEASURES: Platelet uptake was measured using 111Indium-labelled platelets. Restenosis was assessed by repeat angiography at 3 months and clinical symptoms up to 12 months. RESULTS: Median changes in platelet uptake were similar in the three treatment groups, but all platelet radioactivity ratios > 2.0 occurred in the control group. Restenosis at 3 months was observed in 3 control, 5 aspirin and 1 iloprost patient. Further surgical intervention was performed in 3 control and 3 aspirin patients, but in none of the iloprost patients up to 12 months after angioplasty. CONCLUSIONS: Antiplatelet therapy may prevent large increases in platelet deposition at the angioplasty site, but the link between platelet deposition and restenosis was not substantiated in this study.

Aged↗
PubMed2004

Intense exercise increases shear-induced platelet aggregation in men through enhancement of von Willbrand factor binding, glycoprotein IIb/IIIa activation, and P-selectin expression on platelets.

Vigorous exercise transiently enhances the risk of primary cardiac arrest. Shear-induced platelet aggregation (SIPA) is an important mechanism in arterial thrombogenesis. This study investigates whether intense exercise affects SIPA, and elucidates mechanisms that underlie SIPA. Eighteen sedentary healthy men engaged in intense exercise (about 80% of maximal oxygen consumption) for 40 min on a bicycle ergometer. Platelet aggregation, binding of von Willebrand factor (vWF) to platelets, and activation of glycoprotein (GP) IIb/IIIa and expression of P-selectin on platelets induced by shear stress were analyzed both before and immediately after exercise. Analytical results demonstrated that: (1). the levels of plasma vWF antigen and activity were enhanced after intense exercise, (2). intense exercise increased either shear- or ristocetin-induced platelet aggregation and was accompanied by an increase in vWF binding to platelets and vWF-mediated GP IIb/IIIa activation at high shear flow, and (3). shear-induced P-selectin expression in the absence or the presence of exogenous vWF was enhanced by intense exercise. Therefore, we conclude that intense exercise promotes the extent of SIPA, possibly by enhancing the ability of vWF to bind to platelets and the subsequent activation of GP IIb/IIIa complexes, as well as the expression of P-selectin in response to shear stress, which in turn may augment the risk of vascular thrombosis.

Adult↗
PubMed1991

Comparison of the actions of some platelet-activating factor antagonists on platelets and aortic smooth muscles.

The pharmacological actions of five platelet-activating factor (PAF) antagonists were compared in rabbit platelets and rat thoracic aorta. In PAF (2 ng/ml)-induced aggregation of washed rabbit platelets, WEB 2086 and WEB 2170 much were more potent inhibitors than BN 52021, kadsurenone and denudatin B, and the IC50 values were calculated to be 0.1, 0.3, 5, 8 and 10 micrograms/ml, respectively. WEB 2086, WEB 2170 and BN 52021 did not affect the platelet aggregation caused by collagen (10 micrograms/ml), ADP (20 microM), arachidonic acid (100 microM) or thrombin (0.1 U/ml). Kadsurenone and denudatin B suppressed ATP release, thromboxane B2 formation and the rise in intracellular calcium of washed rabbit platelets caused by collagen and thrombin, while WEB 2086, WEB 2170 and BN 52021 did not have an effect. Norepinephrine (3 microM) induced a sustained contraction in rat thoracic aorta. Pretreatment with these PAF antagonists (20-100 micrograms/ml) caused inhibition of the aortic contraction in the following order: kadsurenone greater than denudatin B greater than WEB 2086 greater than BN 52021 greater than WEB 2170. In high potassium (60 mM)-induced contraction of rat aorta, kadsurenone and denudatin B caused marked relaxation, while WEB 2086, WEB 2170 and BN 52021 had only a slight effect. It is concluded that WEB 2086, WEB 2170 and BN 52021 are specific PAF antagonists in rabbit platelets, and weak relaxants in rat aorta. Two other PAF antagonists, kadsurenone and denudatin B, may inhibit some aspects of signal transduction, e.g., thromboxane formation or intracellular Ca2+ mobilization in rabbit platelets, and cause vasorelaxation in rat aorta by inhibiting calcium influx.

Animals↗
PubMed1991

Platelet membrane glycoproteins and platelet functions during storage in the presence of a proteinase inhibitor.

The effect of the proteinase inhibitor aprotinin on membrane glycoproteins and functions of platelets stored for 5 days in platelet-rich plasma was tested. Platelet membrane glycoprotein content was determined by flow cytometry or immunoblot techniques using different monoclonal antibodies. ADP- and ristocetin-induced platelet aggregation and adhesion to collagen were tested in parallel. Using the flow-cytometry technique i) a progressive decrease in the percentage of platelets reacting with the different monoclonal antibodies was observed during storage ii) a 30% reduction of the GPIb mean fluorescence intensity (MFI) was observed after 5 days storage while the MFI of the GP IIb-IIIa complex was not modified. Using the immunoblot technique, a decrease in the amount of both the GPIb alpha and the component of Mr 100,000 was observed, while a 50,000 Mr fragment appeared progressively. Platelet adhesion and aggregation were reduced after 24 hours of storage. Aprotinin prevented neither the GPIb alpha reduction nor the modifications of the functions of human platelets stored in their autologous plasma.

Aprotinin↗
PubMedDate not supplied

Characterization of canine platelet P-selectin (CD 62) and its utility in flow cytometry platelet studies.

1. P-selectin (PADGEM, GMP140, or CD62) a member of lectin-like adhesive proteins is expressed on the surface of activated degranulated canine platelets and is the calcium-dependent receptor for leukocyte adhesion. 2. The electrophoretic mobility of P-selectin, by Western blot analysis and immunoprecipitation from radiolabeled membranes of canine and human platelets, was similar or identical and immunocytochemical studies localized P-selectin in internal vesicles similar to the alpha granule localization in human platelets. 3. Two antibodies to human P-selectin KC4.1 and AC1.2 crossreacted with canine platelets whose surface binding, in response to agonists thrombin, calcium ionophore (A23187), phorbol esters and ADP, was similar. 4. Anti-P-selectin antibodies in conjunction with crossreacting anti-GPIIb/IIIa antibodies (A2A9, 7E3, RUU-PL7F12) enables the analysis of activated platelets, platelet-derived microparticles and platelet-leukocyte interactions in canine models by flow cytometry.

Adenosine Diphosphate↗
PubMed2000

Different role of platelet glycoprotein GP Ia/IIa in platelet contact and activation induced by type I and type III collagens.

The role of glycoprotein Ia/IIa was studied during platelet contact and aggregation induced by type I and type III collagen. The anti-glycoprotein Ia/IIa (6F1) antibody inhibited type I collagen-induced aggregation but did not inhibit the first contact between platelets and collagen. In contrast, it was without effect either on type III collagen-induced contact or platelet interaction with the subendothelium in a static assay. Platelet aggregation induced by type III collagen was only slightly slowed down by 6F1 but pp72 spleen tyrosine kinase phosphorylation was not modified even at concentrations of 6F1 that completely blocked platelet activation induced by type I collagen. Our results indicate that glycoprotein Ia/IIa is not a primary binding site for type I or type III collagen on the platelet membrane. This receptor is more specifically involved in type I collagen-induced platelet spreading and aggregation.

Antibodies, Monoclonal↗
PubMed2001

Variability in platelet responses to collagen--comparison between whole blood perfusions, traditional platelet function tests and PFA-100.

The purpose of this study was to determine if the results obtained in platelet function tests and whole blood perfusions are associated with those in platelet function analyser (PFA)-100. We used collagen type I monomers and fibrils to analyse the distinct roles of glycoprotein (GP) Ia/IIa and other collagen receptors in flowing blood under a high shear rate (1600/s) and in aggregation studies. Also, anticoagulation [citrate vs. D-phenylalanyl-1-prolyl-1 arginine chloromethyl ketone (PPACK)] was varied to enhance the functions of GP Ia/IIa, since it has been shown that the cation-poor environment of citrated blood impairs GP Ia/IIa-dependent platelet recruitment. Large interindividual variability (45-fold) was detected in deposition of platelets in whole blood perfusions over collagen monomers, whereas this variation was only fourfold in fibrils. In PFA, this variation was reduced to 2.5-fold. However, platelet deposition on monomers is associated with epinephrine-enhanced PFA (r=-.49, P<.03), whereas platelet deposition on fibrils is correlated with adenosine diphosphate (ADP)-enhanced PFA (r=-.47, P<.05), suggesting a distinct synergism between epinephrine and monomers (GP Ia/IIa) as well as ADP with fibrils (other collagen receptors). Donors with 807 C/C polymorphism of GP Ia (n=14) had longer lag phase in aggregation experiments compared with C/T (n=7) both by monomers and fibrils (P<.04), but these polymorphisms with their mild impact on GP Ia/IIa activity did not markedly differ in other tests. In conclusion, the results obtained in perfusion studies and PFA experiments correlated, but PFA fails to reveal the large-scale variability related to collagen-induced platelet responses.

Adenosine Diphosphate↗
PubMed2002

Anti-platelet antibodies associated with the Canale-Smith syndrome bind to the same platelet glycoprotein complexes as those of idiopathic thrombocytopenic purpura patients.

The Canale-Smith syndrome (CSS) is an inherited disease characterized by massive lymphadenopathy, hepatosplenomegaly and systemic autoimmunity to erythrocytes and platelets. Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease in which approximately 60-80% of patients have anti-platelet antibodies directed against specific platelet glycoprotein complexes (GPCs) located on their membrane: GP IIb/IIIa, GPIb/IX, and GPIa/IIa. Almost all (95-100%) of the antibody-positive patients have antibodies directed against GPIIb/IIIa alone, or in combination with other glycoprotein targets. Our objective was to determine the specificities of the anti-platelet antibodies in CSS patients. The detection of anti-platelet antibodies was performed using a commercially available ELISA, the Pak-AUTO (GTI, Brookfield, WI), in which highly purified GPIIb/IIIa, GPIb/IX, and GPIa/IIa are immobilized on microtitre plates, incubated with serum or plasma, and subsequently developed with an antihuman polyclonal immunoglobulin. Of 14 CSS patients tested, 11 (79%) had anti-platelet antibodies in their serum directed toward at least one of the three major GPC, nine (82%) of which were against GPIIb/IIIa alone or in combination. Antibodies detected in the sera of ITP patients had similar specificities. No such antibodies were detected in samples from 25 consecutive normal controls. These results demonstrate that a genetically defined defect in lymphocyte apoptosis results in a humoral autoimmune response with anti-platelet specificities very similar to the common idiopathic form of autoimmune thrombocytopenia.

Adolescent↗
PubMed1998

IgG platelet antibodies in EDTA-dependent pseudothrombocytopenia bind to platelet membrane glycoprotein IIb.

EDTA-dependent pseudothrombocytopenia (PTCP) consists of an inappropriate low platelet count caused by autoantibodies present in the serum samples reacting with platelets only in EDTA-anticoagulated blood. By using immunoprecipitation and Western blot techniques, we studied the immunochemical specificity of platelet agglutinating autoantibodies in the serum samples of 10 patients with PTCP. Furthermore, to evaluate a possible role of PTCP-associated IgG autoantibodies in increased platelet turnover, we assayed the plasma glycocalicin (GC) level and calculated the GC index for every patient. Our results provide direct evidence that an epitope located on platelet membrane glycoprotein IIb is recognized by PTCP-associated IgG antibodies; moreover GC levels in patients with EDTA-dependent PTCP were similar to control levels, thus excluding an increased platelet turnover. We conclude that antiplatelet antibodies directed against platelet cryptantigens are unlikely to have a major role in the increased removal of cells from circulation.

Antibodies, Monoclonal↗
PubMed1985

Bleeding disorder associated with albumin-dependent partial deficiency in platelet thromboxane production. Effect of albumin on arachidonate metabolism in platelets.

The authors describe a patient with a longstanding bleeding disorder associated with impaired platelet aggregation and secretion despite normal granule contents. Thrombin-induced platelet thromboxane A2 production, measured using a radioimmunoassay for thromboxane B2, was markedly decreased or undetectable in platelet-rich plasma and whole blood serum. However, significant amounts of thromboxane B2 were detected on thrombin stimulation of platelets suspended in albumin-free salt medium. Malondialdehyde and 14C-hydroxyheptadecatrienoic acid production was undetectable in the patient's platelets. Liberation of free 14C-arachidonic acid from phospholipids during stimulation of prelabeled platelets was normal, indicating normal phospholipase activity. These observations indicate an albumin-dependent partial deficiency in thromboxane production resulting from a defect either in cyclooxygenase or thromboxane synthetase. Further, the authors studied the effect of albumin on arachidonic acid metabolism in normal platelets. These studies indicate that albumin enhances liberation of arachidonic acid from phospholipids but has an overall inhibitory effect on thromboxane synthesis.

Adult↗
PubMed1997

Does the platelet-activated clotting test (HemoSTATUS) predict blood loss and platelet dysfunction associated with cardiopulmonary bypass?

Platelet dysfunction is a major cause of bleeding after cardiopulmonary bypass (CPB). No timely, simple, point-of-care determinant of platelet function is available for clinical use. Adding platelet-activating factor to conventional activated clotting time methods (platelet-activated clotting test [PACT]) (HemoSTATUS; Medtronic, Inc., Parker, CO) produces rapid results (<3 min) and may yield a measure of platelet responsiveness and whole blood procoagulant activity. Blood samples were drawn for PACT, platelet count, prothrombin time, activated partial thromboplastin time, and thromboelastogram (TEG) from 200 patients undergoing cardiac surgery. The PACT significantly decreased from the baseline to postprotamine time interval (P < 0.001). The PACT correlated with 4-h mediastinal blood loss (r = -0.30, P = 0.014). The TEG maximum amplitude also correlated with 4-h mediastinal blood loss (r = -0.32, P = 0.003). The PACT had a sensitivity and specificity comparable to routine laboratory coagulation tests in predicting blood loss. The TEG maximum amplitude, however, was more predictive than both the PACT and routine coagulation tests in this respect. The PACT may be a useful indicator of platelet responsiveness or whole blood procoagulant activity, but we did not find it superior to other tests of coagulation function for predicting excessive blood loss after CPB.

Adult↗
PubMedDate not supplied

Tirofiban administration attenuates platelet and platelet-neutrophil conjugation but not neutrophil degranulation during in vitro VAD circulation.

Ventricular Assist Devices (VADs) have been used as bridges to heart transplantation. However, VAD circulation is complicated by the incidence of thromboembolism, prolonged bleeding, and activation of the inflammatory cascade. We hypothesize that platelet and neutrophil activation are interrelated and linked to the activation of the glycoprotein (GP) IIb/IIIa platelet receptor. The purpose of this study is to evaluate the effects of Tirofiban, a platelet GP IIb/IIIa receptor inhibitor, on platelet and neutrophil activation during simulated VAD circulation. Two groups of five in vitro VAD circuits were simulated with and without Tirofiban using 450 cc of human blood. Blood samples were drawn at specific time intervals up to 72 hours, measuring leukotriene C4 (LTC4), platelet factor four (PF4), and neutrophil elastase. Tirofiban decreased serum levels of PF4 and LTC4 during VAD circulation. Neutrophil elastase secretion was not affected by Tirofiban administration. Preconditioning of VAD circulation with Tirofiban attenuated platelet activation as demonstrated by a decrease in serum PF4 levels. Tirofiban administration ameliorates the inflammatory response by altering platelet-neutrophil interaction as demonstrated by a decrease in LTC4 production. Continued elastase secretion indicates that the inflammatory response is not completely inhibited by Tirofiban administration. These results suggest that neutrophils may be activated by alternative mechanisms. Early complement activation has been demonstrated during in vivo and in vitro VAD circulation and may play a role in mediating inflammatory and thromboembolic reactions during VAD use.

Blood Platelets↗
PubMed2004

Ex vivo evaluation of erythrocytosis-enhanced platelet thrombus formation using the cone and plate(let) analyzer: effect of platelet antagonists.

Red blood cells (RBC) contribute significantly to haemostasis and thrombosis under oscillatory flow conditions, and erythrocytosis has been associated with increased thrombotic risk. To measure the dynamic influences of RBC on platelets, we used a recently described cone and plate(let) analyzer (CPA), evaluating the effect of haematocrit (Hct) on platelet function in whole blood under arterial flow conditions (1800/s, 2 min, 25 degrees C). Anticoagulated blood, reconstituted to varying haematocrits with autologous RBC, demonstrated a significant increase in adherent platelet aggregate formation at Hct levels >45%. This increase was not affected by pretreatment of blood with 0.05 mmol/l aspirin, but was prevented by antagonists of P2Y1, P2Y12, or P2X1, ADP and ATP receptors, and by converting exogenous ADP to ATP with creatine phosphate/creatine phosphokinase. As negligible platelet granule secretion was measured during CPA analysis, but metabolic inhibition of RBC with sodium azide or glutaraldehyde fixation inhibited erythrocytosis-enhanced increases in platelet aggregate size, adenine nucleotides contributing to shear-induced platelet aggregate formation appear to be derived from erythrocytes. These findings support the use of CPA for ex vivo evaluation of the contribution of RBC to platelet function and its inhibition under physiological shear conditions.

Anticoagulants↗