Platelet Aggregation in Whole Blood Determined Using the Ultra-Flo 100 Platelet Counter

Fox, Susan C.; Burgess-Wilson, M.E.; Heptinstall, Stan; Mitchell, J. R. A.

doi:10.1055/s-0038-1657292

Cited by 124 publications

(67 citation statements)

References 5 publications

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“…Experiments were completed within 2 hours after blood was drawn. Whole blood platelet aggregation was measured using the single-platelet counting technique described by Heptinstall et al 16 with the following modifications. Aliquots (400 L) of anticoagulated blood samples were placed into aggregometer cuvettes.…”

Section: Platelet Aggregation and Shape Change In Whole Bloodmentioning

confidence: 99%

“…Aliquots (15 L) before and after agonist addition were removed and placed in 30 L fixing solution containing 0.16% (wt/vol) formaldehyde as described. 16 After dilution, the samples were counted using a platelet counter (Sysmex Platelet Counter PL-100, TOA Medical Electronics, Kobe, Japan) and percentage aggregation calculated as percentage loss of single platelets compared to baseline count. All platelet counts were done in duplicate.…”

Section: Platelet Aggregation and Shape Change In Whole Bloodmentioning

confidence: 99%

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The plaque lipid lysophosphatidic acid stimulates platelet activation and platelet-monocyte aggregate formation in whole blood: involvement of P2Y1 and P2Y12 receptors

Haserück

Erl

Pandey

et al. 2004

Blood

112

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Despite the fact that lysophosphatidic acid (LPA) has been identified as a main platelet-activating lipid of mildly oxidized low-density lipoprotein (LDL) and human atherosclerotic lesions, it remains unknown whether it is capable of activating platelets in blood. We found that LPA at concentrations slightly above plasma levels induces platelet shape change, aggregation, and platelet-monocyte aggregate formation in blood. 1-alkyl-LPA (16:0 fatty acid) was almost 20-fold more potent than 1-acyl-LPA (16:0). LPA directly induced platelet shape change in blood and platelet-rich plasma obtained from all blood donors. However, LPA-stimulated platelet aggregation in blood was donor dependent. It could be completely blocked by apyrase and antagonists of the platelet adenosine diphosphate (ADP) receptors P2Y 1 and P2Y 12 . These substances also inhibited LPA-induced aggregation of platelet-rich plasma and aggregation and serotonin secretion of washed platelets. These results indicate a central role for ADP-mediated P2Y 1 and P2Y 12 receptor activation in supporting LPA-induced platelet aggregation. Platelet aggregation and platelet-monocyte aggregate formation stimulated by LPA was insensitive to inhibition by aspirin. We conclude that LPA at concentrations approaching those found in vivo can induce platelet shape change, aggregation, and platelet-monocyte aggregate formation in whole blood and suggest that antagonists of platelet P2Y 1 and P2Y 12 receptors might be useful preventing LPA-elicited thrombus formation in patients with cardiovascular

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Section: Platelet Aggregation and Shape Change In Whole Bloodmentioning

confidence: 99%

Section: Platelet Aggregation and Shape Change In Whole Bloodmentioning

confidence: 99%

The plaque lipid lysophosphatidic acid stimulates platelet activation and platelet-monocyte aggregate formation in whole blood: involvement of P2Y1 and P2Y12 receptors

Haserück

Erl

Pandey

et al. 2004

Blood

112

View full text Add to dashboard Cite

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“…When citrated whole blood is stirred or mixed in some other way, spontaneous platelet aggregation occurs as a result of platelet activation [1][2][3][4]. A hematology analyzer (CELL-DYN Sapphire Hematology System ® ; Abbott Diagnostics, Abbott Park, IL) [5] with a newly developed software package can specifically count the number of platelet aggregates (PA) in citrated whole blood.…”

Section: Introductionmentioning

confidence: 99%

Platelet aggregation in citrated whole blood of the first trimester of pregnancy

Umazume

Yamada

Morikawa

et al. 2015

Clinica Chimica Acta

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It was recently suggested that platelet reactivity is reduced in early pregnancy. This study was performed to determine whether the citrated whole blood from 33 pregnant women in first trimester showed spontaneous platelet aggregation and whether it differed in extent from that of 11 non-pregnant women. Platelet count and number of platelet aggregates (PA) were serially determined in the same citrated whole blood specimens at 15, 30, 45, 60, 75, and 90 minutes after blood sampling using a hematology analyzer. The number of PA increased significantly at 30 minutes and thereafter in both groups, but was consistently lower for pregnant than non-pregnant women over the 90-minute observation period. The platelet count decreased significantly in a time-dependent manner in both groups, but was significantly lower at 30 and 90 minutes for non-pregnant than pregnant women. The number of PA showed a significant positive correlation with net decrease in platelet count for both pregnant and non-pregnant women. PA counts were also significantly positively correlated with mean platelet volume. In conclusion, platelet reactivity monitored by the increase in number of PA and the fall in platelet count was reduced in early pregnancy compared with non-pregnant healthy controls. (194 words) Key words: mean platelet volume, platelet reactivity, pregnancy, spontaneous platelet aggregation, venous thromboembolism Highlights  Extent of spontaneous platelet aggregation (SPA) was examined. Pregnant women in first trimester were compared with healthy controls. The SPA was less likely to occur in pregnant women. Fall in platelet count was greater in healthy controls. Thus, platelet reactivity was reduced in early pregnancy.

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“…The recovery of known amounts of added blood was 96.8 ± 0.6%. Studies of platelet function in whole blood were carried out using the method of Fox et al (1982). Briefly, spontaneous platelet aggregation was determined during stirring in response to: adenosine diphosphate 0.5 FM, adrenaline bitartrate 0.1-1.0 RM, thrombin 0.05 u ml-1 and sodium arachidonate 0.1-0.2 mm (all from Sigma Co Ltd, Poole, Dorset).…”

Section: Methodsmentioning

confidence: 99%

“…The subjects in the non-pregnant studies were all male, and the dose per kilogram bodyweight will have been some 20% higher in the patients of this paper. In this study, using whole-blood aggregometry (Fox et al, 1982) (Fritschka et al, 1986;Dale et al, 1983 …”

Section: Plasma Nitrendipine Concentrationsmentioning

confidence: 99%

Some observations on the effects of a calcium channel blocker, nitrendipine, in early human pregnancy.

Lawrence

Pipkin

1987

Brit J Clinical Pharma

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The effects of a dihydropyridine calcium channel antagonist, nitrendipine 20 mg orally, have been investigated in 24 women in the first trimester human pregnancy in a double‐blind, placebo controlled study. The effects on systemic arterial pressure, pulse rate (PR), blood loss at termination of pregnancy (TOP), plasma renin, renin substrate and aldosterone concentrations and platelet aggregation to adenosine diphosphate 0.5 microM, adrenaline bitartrate 0.1‐1.0 microM, thrombin 0.05 u ml‐1 and sodium arachidonate 0.1‐0.2 mM were studied. Administration of nitrendipine was associated with a statistically‐ significant fall in diastolic pressure (BPD) the magnitude of which was directly related to the individual peak concentrations of the drug (P less than 0.02). No significant effects were observed on systolic pressure (BPS);PR rose slightly. Baseline variability of all three parameters fell in the nitrendipine‐treated group over the first 2 h but then increased significantly (BPS, P less than 0.05; BPD, P less than 0.025; PR, P less than 0.005). There was a positive association in both placebo and treated groups between the rates of change of BPD and PR (P less than 0.005 for both); nitrendipine exerted a highly significant (P less than 0.001) effect on this association compatible with its effect as a vasodilator. Blood loss consequent on TOP did not differ in the two groups (nitrendipine 104 +/‐ 16 ml; placebo 114 +/‐ 20 ml). There were no significant differences in basal or stimulated hormone concentrations in the two groups. The ex vivo platelet aggregatory response in whole blood to 0.1 mM sodium arachidonate was inhibited by nitrendipine (P less than 0.05); responsiveness to the other aggregatory agents studied was not changed. There was a wide individual variation in both time to peak concentration of nitrendipine and the size of the peak, making classical pharmacokinetic analysis impossible. The median time after ingestion to peak concentration was 105 min; the median concentration was 7.8 ng ml‐1. These data suggest that, in the context of the severe vasoconstriction and platelet aggregability of pregnancy‐induced hypertension, further studies of this drug in pregnancy are warranted.

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Platelet Aggregation in Whole Blood Determined Using the Ultra-Flo 100 Platelet Counter

Cited by 124 publications

References 5 publications

The plaque lipid lysophosphatidic acid stimulates platelet activation and platelet-monocyte aggregate formation in whole blood: involvement of P2Y1 and P2Y12 receptors

The plaque lipid lysophosphatidic acid stimulates platelet activation and platelet-monocyte aggregate formation in whole blood: involvement of P2Y1 and P2Y12 receptors

Platelet aggregation in citrated whole blood of the first trimester of pregnancy

Some observations on the effects of a calcium channel blocker, nitrendipine, in early human pregnancy.

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