The Filtragometer: A New Device for Measuring Platelet Aggregation in Venous Blood of Man

1975 ◽  
Vol 34 (02) ◽  
pp. 531-544 ◽  
Author(s):  
G Hornstra ◽  
F ten Hoor
Keyword(s):  
Platelet Aggregation ◽  
Pressure Difference ◽  
Venous Blood ◽  
New Device ◽  
Platelet Aggregates ◽  
Spontaneous Platelet Aggregation ◽  
Short Time ◽  
Forearm Vein

SummaryA new device for the direct assessment of spontaneous platelet aggregation in human venous blood is described: the Filtragometer. The principle of the method is based on measurement of the pressure difference across a filter with pores of 20 μπι diameter through which blood from a forearm vein is drawn. Platelet aggregates, obstructing the filter, cause a change in the pressure difference which is proportional to the degree of platelet aggregation. The measurement takes only a short time and a small amount (5-10 ml) of blood.Platelet aggregation as measured with the Filtragometer depends on the type of anticoagulant used. The Filtragometer response decreases on inhibition of platelet stickiness in vitro by prostaglandin E1 and in vivo by aspirin ingestion. Moreover it appeared to be higher in a group with a high thrombosis tendency than in a group less susceptible to fatal arterial thrombosis.The Filtragometer seems especially useful in monitoring the results of diet and/or drug therapy.

Accumulation of Macromolecular Particles in the Reticuloendothelial System (RES) Mediated by Platelet Aggregation and Disaggregation

1969 ◽  
Vol 22 (03) ◽  
pp. 496-507 ◽  
Author(s):  
W.G van Aken ◽  
J Vreeken
Keyword(s):  
Platelet Aggregation ◽  
Degradation Products ◽  
Reticuloendothelial System ◽  
Caproic Acid ◽  
Carbon Particles ◽  
Carbon Clearance ◽  
Aggregation And Disaggregation ◽  
Platelet Aggregates

SummaryCarbon particles cause platelet aggregation in vitro and in vivo. Prior studies established that substances which modify thrombocyte aggregation also influence the rate at which carbon is cleared from the blood.This study was performed in order to elucidate the mechanism by which the carbon-platelet aggregates specifically accumulate in the RES.Activation of fibrinolysis by urokinase or streptokinase reduced the carbon clearance rate, probably due to generated fibrinogen degradation products (FDP). Isolated FDP decreased the carbon clearance and caused disaggregation of platelets and particles in vitro. Inhibition of fibrinolysis by epsilon-amino-caproic acid (EACA), initially accelerated the disappearance of carbon and caused particle accumulation outside the RES, predominantly in the lungs. It is supposed that platelet aggregation and locally activated fibrinolysis act together in the clearance of particles. In the normal situation the RES with its well known low fibrinolytic activity, becomes the receptor of the particles.

scholarly journals Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 205-209 ◽  
Author(s):  
FH Kohanna ◽  
MH Smith ◽  
EW Salzman
Keyword(s):  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Thromboembolic Disease ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Lower Ratio

Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

Influence of Fibrinogen Split Products on Platelets

1967 ◽  
Vol 17 (01/02) ◽  
pp. 078-098 ◽  
Author(s):  
M. I Barnhart ◽  
D. C Cress ◽  
R. L Henry ◽  
J. M Riddle
Keyword(s):  
Platelet Aggregation ◽  
Plasma Concentration ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Platelet Response ◽  
Transient Nature ◽  
Platelet Morphology ◽  
Platelet Aggregates

SummaryBreakdown products of fibrinogen and fibrin can play a role in hemostasis and also may be of consequence in thrombosis. β2 fibrinogen derivative D is an electropositive terminal proteolysis product of fibrinolysis which has the ability to aggregate platelets. The normal plasma concentration of such nonclottable fibrinogen relatives is 0.2 mg/ml. During fibrinolysis this concentration may reach 5 mg/ml plasma. Addition of β 2 fibrinogen D (raising the plasma concentration 0.1 to 5 mg/ml) either in vivo or in vitro induced platelet aggregations. Moreover, alterations in platelet morphology occurred which were obvious by electron microscopy.Platelet depletion was a consistent response to the infusion of purified β2 fibrinogen D (8 to 55 mg/kg body weight) into dogs. Circulating platelets decreased as much as 85% but were only temporarily aggregated and reappeared in the circulation within 1 to 5 hrs. Small platelet aggregates circulated while large aggregates were trapped in the microcirculation. Thrombin was not responsible for the platelet aggregations as neither prothrombin nor clottable fibrinogen were changed significantly. The transient nature and morphological features of the platelet response according to microscopic criteria were prominent during and after infusion of β2 fibrinogen D.In vitro studies included 3 systems; washed platelets, platelet rich plasma and whole blood. Positive results were obtained with all, but platelets in whole blood were most responsive. The magnitude of platelet aggregation and morphology correlated with the concentration of β2 fibrinogen D. Platelet aggregation induced by ADP (10~5 mg/ml) was compared with that induced by β2 fibrinogen D (0.09 to 0.72 mg/ml). With either reagent aggregates were of dendritic forms. Combination of the 2 reagents was additive but did not further change the morphology. Additional factors seem necessary for development of viscous metamorphosis.

scholarly journals Intratumoral platelet aggregate formation in a murine preclinical glioma model depends on podoplanin expression on tumor cells

2019 ◽  
Vol 3 (7) ◽  
pp. 1092-1102 ◽  
Author(s):  
Barbara Costa ◽  
Tanja Eisemann ◽  
Jens Strelau ◽  
Ingrid Spaan ◽  
Andrey Korshunov ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Tumor Cells ◽  
Cell Types ◽  
Platelet Receptor ◽  
Increased Risk ◽  
Platelet Aggregates ◽  
Glioma Model ◽  
Novel Strategy

Abstract Binding of the sialomucin-like transmembrane glycoprotein podoplanin (PDPN) to the platelet receptor C-type lectin-like receptor 2 induces platelet activation and aggregation. In human high-grade gliomas, PDPN is highly expressed both in tumor cells and in tumor-associated astrocytes. In glioma patients, high expression of PDPN is associated with worse prognosis and has been shown to correlate with intratumoral platelet aggregation and an increased risk of venous thromboembolism (VTE). To functionally assess the role of PDPN in platelet aggregation in vivo, we established a syngeneic orthotopic murine glioma model in C57/Bl6 mice, based on transplantation of p53- and Pten-deficient neural stem cells. This model is characterized by the presence of intratumoral platelet aggregates and by the upregulation of PDPN both in glioma cells and in astrocytes, reflecting the characteristics of human gliomas. Deletion of PDPN either in tumor cells or in astrocytes resulted in glioma formation with similar penetrance and grade compared with control mice. Importantly, only the lack of PDPN in tumor cells, but not in astrocytes, caused a significant reduction in intratumoral platelet aggregates, whereas in vitro, both cell types have similar platelet aggregation-inducing capacities. Our results demonstrate a causative link between PDPN and platelet aggregation in gliomas and pinpoint the tumor cells as the major players in PDPN-induced platelet aggregation. Our data indicate that blocking PDPN specifically on tumor cells could represent a novel strategy to prevent platelet aggregation and thereby reduce the risk of VTE in glioma patients.

Spontaneous Platelet Aggregation in Arterial Insufficiency: Mechanisms and Implications

1976 ◽  
Vol 35 (03) ◽  
pp. 702-711 ◽  
Author(s):  
Kenneth K. Wu ◽  
John C. Hoak
Keyword(s):  
Platelet Aggregation ◽  
Normal Subjects ◽  
Low Concentrations ◽  
Vascular Insufficiency ◽  
Arterial Insufficiency ◽  
High Concentrations ◽  
Peripheral Arterial ◽  
Spontaneous Platelet Aggregation

SummaryTo investigate the clinical implications and mechanisms of spontaneous platelet aggregation (SPA) in man, 150 normal subjects, 22 patient controls and 130 patients with vascular insufficiency were studied. SPA was negative in normal subjects and patient controls whereas it was positive in 36 of 66 (54%) patients with transient ischemic attacks, 6 of 32 (19%) patients with stable angina, 7 of 10 (70%) patients with acute myocardial infarction and 11 of 14 (80%) patients with acute peripheral arterial insufficiency. The SPA was inhibited with aspirin in vivo, and inhibited competitively in vitro by low concentrations of aspirin, 2-chloroadenosine, prostaglandin E1 or apyrase but only by high concentrations of heparin or hirudin. Addition of platelet-poor plasma from patients with positive SPA did not cause normal platelets to aggregate. Treatment of patients who had acute peripheral arterial insufficiency with aspirin and dipyridamole prevented SPA with notable clinical improvement of the ischemic changes.

Platelet Aggregation Induced In Vivo By Heparin And Heparin Fractions

1981 ◽  
Author(s):  
M Silane ◽  
J N Lindon ◽  
B J Ransil ◽  
R D Rosenberg ◽  
E W Salzman
Keyword(s):  
Molecular Weight ◽  
Platelet Aggregation ◽  
Reciprocal Relationship ◽  
Low Molecular Weight ◽  
Arterial Blood ◽  
Platelet Aggregate ◽  
Heparin Fractions ◽  
Platelet Aggregates

As we have reported, heparin-induced platelet aggregation in vitro varies among heparin subfractions, being generally less with lower molecular weights and having a reciprocal relationship with antithrombin affinity.We now have studied heparin-induced platelet aggregates in vivo by the technique of Wu and Hoak using arterial blood from unanesthetized rabbits. Porcine mucosal heparin was fractionated by gel filtration into high molecular weight (ave. 15,000 Daltons) or low molecular weight (ave. 6,000 Daltons) preparations. IV administration of commercial porcine mucosal heparin (spec. act. 150 u/mg) or high (spec. act. 183 u/mg) or low (spec. act. 208 u/mg) molecular weight fractions was followed by an increase in the platelet aggregate ratio compared with preinjection control values. The rise in platelet aggregate ratio with heparin was significantly different from the effect of a saline placebo (n=8) but was not significantly different among rabbits receiving the commercial heparin (n=9) or the high (n=8) or low (n=8) molecular weight preparations. Peak rise in circulating aggregate ratio occurred 2 minutes after the injection, and values returned to control levels within 15 to 30 minutes. There was no change in platelet count in blood collected in EDTA, suggesting that the aggregates were not removed from the circulation in vivo.Heparin fractions of low molecular weight were further separated according to antithrombin affinity by an antithrombin binding technique. In 8 rabbits low molecular weight/high antithrombin affinity heparin (spec. act. 480 u/mg) did not cause formation of platelet aggregates. The results were significantly different from those with commercial heparin (p=0.05) or with the other heparin fractions (p=0.06).Clinical use of low molecular weight heparin of high antithrombin affinity may lead to fewer heparin-induced platelet effects and to an improvement in anticoagulant therapy.

STREPTOKINASE-INDUCED, ANTIBODY-MEDIATED PLATELET AGGREGATION: A POTENTIAL CAUSE OF CLOT PROPAGATION IN VIVO

1987 ◽  
Author(s):  
D E Vaughan ◽  
J Loscalzo
Keyword(s):  
Platelet Aggregation ◽  
Index Case ◽  
Platelet Rich Plasma ◽  
The Past ◽  
Neutralizing Capacity ◽  
Tissue Plasminogen ◽  
Spontaneous Platelet Aggregation ◽  
Induced Aggregation

We identified a patient who exhibited paradoxical propagation of thrombus coincident with the administration of intracoronary streptokinase (SK) that was mediated by anti-SK antibodies. The patient had not been treated with SK in the past and had a plasma SK-neutralizing capacity of 160 U/ml. Using platelet-rich plasma (PRP) obtained from the patient, we found that SK initiated spontaneous platelet aggregation and secretion in vitro. Aggregation was specific for SK and not induced by urokinase or tissue plasminogen activator. In 14 of 15 controls, no platelet aggregation was observed in PRP with addition of SK. The addition of plasma or purified IgG from our index case to the PRP of all 14 controls supported SK-induced aggregation. This aggre-gatory response was not inhibited by aprotinin. Using purified proteins in a washed platelet system, we found that platelet aggregation was dependent on the presence of SK, specific anti-SK IgG, plasminogen, and platelets. These data demonstrate that anti-SK antibodies can promote platelet aggregation, presumably by binding to platelet-bound plasminogen-SK complexes. These data also imply that some individuals may possess anti-SK antibodies that are capable of inducing platelet aggregation in vivo and, thereby, promoting clot propagation or thromboembolic complications. In the absence of adequate, specific screening, this observation argues for the use of nonimmunogenic thrombolytic agents in the emergent setting.

Platelet Function in Childhood Migraine

Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 99-101 ◽  
Author(s):  
Pietro Carrieri ◽  
Fulvio Sorge ◽  
Giuseppe Orefice ◽  
Salvatore De Feo
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Plasma Levels ◽  
Childhood Migraine ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates

Platelet function in vitro and in vivo (ADP-induced platelet aggregation, circulating platelet aggregates, β-thromboglobulin plasma levels) has been studied in children with common migraine, in headache-free intervals. Migraine patients demonstrated increased circulating platelet aggregates when compared with controls. Moreover, two of ten patients had pathological β-thromboglobulin levels. These data indicate that in some children with migraine there is an abnormality of platelet function during headache-free periods.

scholarly journals Type IIB Tampa: a variant of von Willebrand disease with chronic thrombocytopenia, circulating platelet aggregates, and spontaneous platelet aggregation

Blood ◽  
1985 ◽  
Vol 66 (2) ◽  
pp. 282-286 ◽  
Author(s):  
HI Saba ◽  
SR Saba ◽  
J Dent ◽  
ZM Ruggeri ◽  
TS Zimmerman
Keyword(s):  
Platelet Aggregation ◽  
Von Willebrand Factor ◽  
Von Willebrand Disease ◽  
New Variant ◽  
Platelet Aggregate ◽  
Spontaneous Platelet Aggregation ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Type IIB von Willebrand disease is characterized by enhanced ristocetin- induced platelet aggregation and absence of large von Willebrand factor multimers from plasma. An alteration of the von Willebrand factor molecule resulting in increased reactivity with platelets appears to be the basis for these abnormalities. We have now identified a new variant of type IIB von Willebrand disease in a family in which the four affected members also have chronic thrombocytopenia, in vivo platelet aggregate formation, and spontaneous platelet aggregation in vitro. In spite of repeatedly prolonged bleeding times and persistent thrombocytopenia, their bleeding diathesis is only moderate.

scholarly journals Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 205-209 ◽  
Author(s):  
FH Kohanna ◽  
MH Smith ◽  
EW Salzman
Keyword(s):  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Thromboembolic Disease ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Lower Ratio

Abstract Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

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