Functional Fractionation of Platelets: Aggregation Kinetics and Glycoprotein Labeling of Differing Platelet Populations

Haver, Virginia M.; Gear, Adrian R.L.

doi:10.1055/s-0038-1657259

Cited by 17 publications

(14 citation statements)

References 10 publications

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“…Large platelets were more sensitive to ADP than small platelets, with a lower K,, but surprisingly aggregated less rapidly, as evidenced by a lower B/,,,. We reached a similar conclusion when platelets were first separated on the basis of their sensitivity to ADP and then subjected to kinetic analysis (Haver and Gear 1982). Such kinetic data can help clarify the problems of platelet heterogeneity and differential hnctiond efficiency of subpopulations.…”

Section: Figmentioning

confidence: 59%

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Platelet adhesion, shape change, and aggregation: rapid initiation and signal transduction events

Gear

1994

Can. J. Physiol. Pharmacol.

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GEAR, A.W.L. 1994. Platelet adhesion, shape change, and aggregation: rapid initidion and signal transduction events. Can.J. Physiol. Phamcol. 72: 28% -294. Blood platelets are essential for hemostasis, and knowledge of their function is important for understanding both normal and pathologic situations. A number of approaches have been used to evaluate platelet adhesion, aggregation, and secretion, and within the last Id) years much interest has been directed to the biochemical mechanisms and signal transduction events wcurring during these various phases of function. New information has come from development of technologies to evaluate the changes occurring immediately after platelet activation and consistent with the speed needed for hemostasis in the arterial circulation. Use of rapid flow and mixing technologies as seen in quenched-flow, continuous-flow, and stopped-flow devices has revealed that platelet aggregation, shape change, adhesion, and secretion begin within 1 s and may be nearly complete by 5 s. Biochemical changes such as in protein phosphorylation, calcium release, and phospholipid hydrolysis are clearly evident in hundreds of milliseconds. Therefore, it is necessary to understand these early events in signal transduction and to assess alterations that may occur in diseases such as diabetes.Key rwkards: platelets, quenched flow, aggregation, adhesion, inositol. GEAR,A.R.L. 1994. Platelet adhesion, shape change, and aggregation: rapid initiation and signal transduction events. Can. J. Physiol. Phamacol. 72 : 285-294. Ees plaquettes sanguines jouent un rdle essentiel dans 19hCmostase, et il est important d'en connaitre la fonction pour comprendre tant Ies situations pathologiques que nomales. Plusieurs apprwhes ont Ct C utilisCes pour Cvaluer 19adhCsion, I'agrCgation et B a sCcr6tion des plaquettes, et, au cours des 18 demikres annCes, un intCr6t particulier a Ct C port6 atax mCcanismes biochimiques et B la phase de transduction des signaux dans ces diverses fonctions. De nouvelles informations ont pu Ctre acquises griice au dCveloppement de techniques pour Cvaluer les variations se produisant immCdiatement aprks l'activation plaquettaire et respectant la vitesse nicessaire ? i 19Ctablissement de 1'hCmostase dans la circulation artbrielle. L'utilisation de dCbit mpide et de techniques de knixage qu'offrent les appreils B Ccoulement bioquC, continu ou stoppant, a rCvClC que l'agrdgation, le changement de fome, I'adhCsion et la sCcrCtion des plaquettes commencent en dedans de 1 s et gourraient $tre presque compldt6s en 5 s. k s manifestations biochimiques, observies par exemple dans la phosphorylation protbinique, la libhation de calcium et l'hydrolyse des phospholipides, se prCsentent en qtaelques centaines de millisecondes. Ainsi, il est nCcessaire de comprendre ces phases prCcoces de la transduction des signaux et d'Cvaluer les altkrations qui pourraienmt se produire dans les maladies comme le diabke.

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Section: Figmentioning

confidence: 59%

“…1 ; Frojmovic 1973). Onset is well within 1 s, and aggregation rates are typically 20 -50 96 of platelets disappearing per second (Gear 1982;Haver and Gear 1982;Carty and Gear 1986). In the inset to Fig.…”

Section: Principle Of Quenched--ow Aggregsrnetrymentioning

confidence: 99%

Platelet adhesion, shape change, and aggregation: rapid initiation and signal transduction events

Gear

1994

Can. J. Physiol. Pharmacol.

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“…Mean platelet volume (MPV) is an indicator of platelet size and has been known to be a marker of platelet activity. Large platelets are more reactive than small platelets and produce more thromboxane A 2 , express more glycoprotein Ib and glycoprotein IIb/IIIa receptors, and aggregate more easily (11,12) . In the present study, we aimed to investigate the platelet activity in the development of RAO through MPV.…”

Section: Introductionmentioning

confidence: 99%

Mean platelet volume in patients with retinal artery occlusion

Şahin¹,

Şahin²,

Yüksel³

et al. 2016

Arquivos Brasileiros De Oftalmologia

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RESUMO Objetivo: O objetivo deste estudo foi investigar o volume plaquetário médio (MPV) de pacientes com oclusão da artéria da retina (RAO ABSTRACTPurpose: The aim of this study was to investigate the mean platelet volume (MPV) of patients with retinal artery occlusion (RAO). Methods: Thirty-seven patients diagnosed with RAO and 32 control subjects were included in this retrospective study. Retinal artery occlusion was diagnosed on the basis of clinical examination and fundus fluorescein angiography. All participants underwent complete ocular examination, and MPV, hematocrit, hemoglobin, and platelet counts were recorded. RAO patient data were compared with those of the control subjects.Results: Patients with RAO had significantly higher MPV values (7.96 ± 1.2 fL) com pared with control subjects (7.33 ± 0.7 fL, p<0.001). No significant difference was found with regard to platelet count between the RAO group and the control group (262 ± 70.1 × 10 9 /L and 251 ± 56.6 × 10 9 /L, respectively, p=0.50). MPV was an independent predictor of RAO [odds ratio (OR)=0.50; 95% confidence interval (CI)=0.28-0.89; p=0.019). Conclusions: Our results demonstrated that MPV values were significantly higher in patients with RAO, suggesting that larger platelets may contribute to the pathogenesis of the RAOs.

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“…The use of platelet-rich plasma for platelet aggre-gation studies has two main disadvantages: first, because platelets are heterogeneous in terms of size, density and metabolic activities [8,9], certain populations of platelets may not be recovered by centrifugation; therefore, the results of aggregation studies on plateletrich plasma may not represent platelet func tion in whole blood; second, in platelet-rich plasma, platelet aggregation occurs in the ab sence of red and white blood cells. We have shown [10] that platelet behaviour in whole blood can be very different from that in platelet-rich plasma.…”

Section: Introductionmentioning

confidence: 99%

Effect of Prostacyclin (Epoprostenol) on the Aggregation of Human Platelets in Whole Blood in vitro

Saniabadi¹,

Lowe²,

Belch³

et al. 1984

Pathophysiol Haemos Thromb

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Prostacyclin (PGI₂) is a potent endogenous inhibitor of platelet aggregation. The effect of PGI₂ on platelet aggregation and disaggregation in whole human blood was studied at 37 °C in vitro. Aggregation or disaggregation was quantified by counting single platelets using the recently developed Ultra Flo 100 Whole Blood Platelet Counter. Aggregation of platelets in whole blood was induced by arachidonic acid (AA, 400 μM), adenosine 5’-diphosphate (ADP, 10 μM), thrombin (0.1 U/ml) and collagen (1 μg/ml). At peak aggregation, each aggregating agent induced about a 90% fall in the number of single platelets counted. When whole blood was pre-incubated with PGI₂ (0.5–8 nM), it dose dependently inhibited aggregation of platelets induced by all four aggregating agents. Platelet aggregates induced by ADP or thrombin could rapidly be disaggregated by PGI₂ added to blood at peak aggregation. Disaggregation of collagen-induced platelet aggregation by PGI₂ was slow and minimal and it was completely ineffective in disaggregating AA-induced platelet aggregates. Unlike platelet-rich plasma, which is routinely used to study platelet aggregation, the present whole-blood method allows red and white blood cells to exert their influences on platelet function, and is an important step towards a physiological state for evaluating the effects of pharmacological agents on platelets in whole blood in vitro and ex vivo.

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Functional Fractionation of Platelets: Aggregation Kinetics and Glycoprotein Labeling of Differing Platelet Populations

Cited by 17 publications

References 10 publications

Platelet adhesion, shape change, and aggregation: rapid initiation and signal transduction events

Platelet adhesion, shape change, and aggregation: rapid initiation and signal transduction events

Mean platelet volume in patients with retinal artery occlusion

Effect of Prostacyclin (Epoprostenol) on the Aggregation of Human Platelets in Whole Blood in vitro

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