In Vivo Platelet Release in Myeloproliferative Disorders

1982 ◽  
Vol 48 (01) ◽  
pp. 041-045 ◽  
Author(s):  
H Ireland ◽  
D A Lane ◽  
S Wolff ◽  
M Foadi
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Plasma Concentrations ◽  
Myeloproliferative Disorders ◽  
Blood Platelet ◽  
Count Ratio ◽  
The Mean ◽  
Platelet Release ◽  
Blood Platelet Count

SummaryThe in vivo platelet release reaction in 22 patients with myeloproliferative disorders has been studied by measuring plasma concentrations of the platelet release product β-throm-boglobulin (βTG). Mean βTG and mean βTG:whole blood platelet count ratio were significantly raised in the patient group taken as a whole compared to an age matched control group. No significant increases were observed in the plasma concentrations of thrombin and plasmin sensitive fibrinogen fragments fibrinopeptide A (FpA) and Bβ1-42. The patients were divided into those who had normal, increased or decreased responses to in vitro ADP-induced platelet aggregation. Mean βTG and the mean βTG:whole blood platelet count ratio were higher in the increased and decreased responders to ADP than in the normal aggregation group, but the differences in means were not statistically significant. Aspirin given to six patients at a dose sufficient to eliminate the secondary phase of ADP-induced platelet aggregation reduced mean βTG and the mean βTG : whole blood platelet count ratio but did not alter mean FpA and Bβ1-42. It is concluded that the enhanced platelet release reaction seen in myeloproliferative disorders is independent of plasma protease activity that arises when coagulation and fibrinolytic systems are activated.

Platelet Aggregation in Rats in Relation to Hyperuricaemia Induced by Dietary Single-Cell Protein and to Protein Deficiency

1978 ◽  
Vol 39 (02) ◽  
pp. 346-359 ◽  
Author(s):  
P D Winocour ◽  
M R Turner ◽  
T G Taylor ◽  
K A Munday
Keyword(s):  
Uric Acid ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Time Lag ◽  
Blood Platelet ◽  
Single Cell Protein ◽  
Cell Protein ◽  
Low Protein ◽  
Blood Platelet Count ◽  
Rat Platelets

SummaryA major limitation to single-cell protein (SCP) as a human food is its high nucleic acid content, the purine moiety of which is metabolised to uric acid. Rats given a Fusarium mould as a source of SCP in diets containing oxonate, a uricase inhibitor, showed elevated plasma and kidney uric acid concentrations after 21 d, which were related to the level of dietary mould. ADP-induced and thrombin-induced platelet aggregation was greater in the hyperuricaemic rats than in controls and a progressive increase in aggregation with increasing levels of dietary mould was observed. Furthermore a time-lag, exceeding the life-span of rat platelets, was observed between the development of hyperuricaemia and the increase in aggregation. A similar time-lag was observed between the lowering of the hyperuricaemia and the reduction of platelet aggregation when oxonate was removed from the diet.If human platelets react to uric acid in the same manner as rat platelets this might explain the link that has been suggested between hyperuricaemia and ischaemic heart disease. In that event diets high in nucleic acids might be contra-indicated in people at risk from ischaemic heart disease.In rats given a low protein diet (50 g casein/kg) for 21 d ADP-induced and thrombin-induced platelet aggregation and whole blood platelet count were reduced compared with control animals receiving 200 g casein/kg diet but not in rats given 90 or 130 g casein/kg diet. A study of the time course on this effect indicated that the reduction both in aggregation tendency and in whole blood platelet count occurred after 4 d of feeding the low protein diet. These values were further reduced with time.

Recovery of Donor Peripheral Blood Platelet Count Following Platelet Apheresis.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2892-2892
Author(s):  
Larry J. Dumont ◽  
L. Lassahn ◽  
Peter A. Tomasulo ◽  
Dennis Harpool ◽  
S. Pinkard ◽  
...  
Keyword(s):  
Platelet Count ◽  
Regression Model ◽  
Peripheral Blood ◽  
De Novo ◽  
Blood Platelet ◽  
Platelet Recovery ◽  
Platelet Release ◽  
Kinetics Of ◽  
Blood Platelet Count

Abstract BACKGROUND: Apheresis platelet collection from healthy normal blood donors can reduce the donor peripheral blood platelet concentration by 50% or more. The kinetics of peripheral blood platelet count (PLT) recovery in the apheresis donors over the first 24 hours has not been described. The objective of this study was to determine the recovery kinetics of the donor peripheral blood platelet count following apheresis platelet donation. METHODS: Healthy apheresis platelet donors were enrolled following informed consent. The apheresis platelet collection was performed using the Gambro Trima system (Gambro BCT, Lakewood, CO) following local SOP and manufacturer’s directions for use. The minimum predicted post-count was configured in the Trima to no less than 78K plt/μL. PLT was determined pre-procedure (Pre), immediately post procedure (Post), 4–11 h (FU1) and 11–41 h (FU2) post-donation using standard methods. The PLT recovery was evaluated as the increase in PLT following the donation (Delta). The effects of study site, time of sample, and the fraction of platelets collected (Fpc) at donation on Delta were evaluated using a random effects generalized linear regression model. A full regression model of Delta as a function of study site, follow-up period and Fpc with all main and interaction effects was used to test hypotheses. RESULTS: 548 subjects were entered into the study at 3 study sites; Pre-PLT 276±59 × 103 plt/μL, Post-PLT 205±47 × 103 plt/μL, Fpc 25±10%. No adverse events were reported by any subjects. Recovery of platelet count following apheresis platelet donation is variable between subjects; and the independent variables of study site, follow-period and Fpc accounted for 25% of the total variation in Delta. PLT increased 12.4±0.9 × 103 plt/μL by the time of follow-up sampling (p=0.01), although there was no difference between PLT at FU1 (214±49 × 103 plt/μL) and FU2 (212±47 × 103 plt/μL; p=0.15). None of the donors reached their pre-donation platelet count during the follow-up period. There was no difference in Delta between centers (p=0.23). Fpc had a significant affect on Delta (p<0.0001); with estimated Delta of 5.2±0.9 × 103 plt/μL at Fpc=15% and 16.0±.8 × 103 plt/μL at Fpc=30%. CONCLUSION: Platelet recovery following apheresis platelet donation was observed to be dependent on the fraction of platelets donated. Surprisingly, the recovery observed within the first 11 h was equivalent to that observed between 11–42 h, averaging 17.5% of the drop observed during apheresis. Recovery was not complete when observed for up to 41 h following donation in this study. Additional investigation of PLT recovery following apheresis donation is indicated to describe and differentiate the potential roles of de novo production, early pro-platelet release and platelet release from peripheral pools over the early post-donation period.

scholarly journals Haemostatic Factors in Umbilical Artery and Vein Blood

1977 ◽  
Author(s):  
M.E. Foley ◽  
J.K. Clayton ◽  
G.P. McNicol
Keyword(s):  
Platelet Count ◽  
Umbilical Artery ◽  
Degradation Products ◽  
Umbilical Vein ◽  
Blood Platelet ◽  
Clotting Factor ◽  
Platelet Factor ◽  
Haemostatic Factors ◽  
The Mean ◽  
Blood Platelet Count

Increased clotting factor activity has been demonstrated by other workers in uterine vein blood at the time of placental separation. To examine some effects of placental separation on the fetus, haemostatic factors in umbilical artery and vein blood were studied immediately following delivery in 80 normal babies. Clotting activity was increased in umbilical vein blood as compared with umbilical artery blood; the most obvious difference was a significant shortening of the activated partial thromboplastin time. Cord blood showed a high level of fibrinolytic activity; activity measured in plasma by the fibrin plate method and with the euglobulin lysis test was significantly greater in the umbilical vein than in the artery. Normal levels of fibrinogen degradation products indicated no active fibrinogenolysis or fibrinolysis. The mean umbilical vein blood platelet count (233 × 109/litre) was significantly higher than the mean umbilical artery blood platelet count (205 × 109/litre). Platelet factor 3 availability showed no arteriovenous difference. Platelet aggregation to 2 and 4 micromolar adenosinediphosphate was significantly greater in the umbilical vein than in umbilical artery blood. The data indicate that at the time of placental separation, there is increased potential haemostatic activity in the fetus.

Do Extra-Platelet Sources Contribute to the Plasma Level of Thrombospondin?

1988 ◽  
Vol 59 (02) ◽  
pp. 273-276 ◽  
Author(s):  
J Dawes ◽  
D A Pratt ◽  
M S Dewar ◽  
F E Preston
Keyword(s):  
Platelet Count ◽  
Background Concentration ◽  
Serum Concentrations ◽  
Bone Marrow Depression ◽  
Serial Sampling ◽  
Control Serum ◽  
Platelet Release ◽  
Highly Correlated ◽  
The Relationship

SummaryThrombospondin, a trimeric glycoprotein contained in the platelet α-granules, has been proposed as a marker of in vivo platelet activation. However, it is also synthesised by a range of other cells. The extraplatelet contribution to plasma levels of thrombospondin was therefore estimated by investigating the relationship between plasma thrombospondin levels and platelet count in samples from profoundly thrombocytopenic patients with marrow hypoplasia, using the platelet-specific α-granule protein β-thromboglobulin as control. Serum concentrations of both proteins were highly correlated with platelet count, but while plasma β-thromboglobulin levels and platelet count also correlated, there was no relationship between the number of platelets and thrombospondin concentrations in plasma. Serial sampling of patients recovering from bone marrow depression indicated that the plasma thrombospondin contributed by platelets is superimposed on a background concentration of at least 50 ng/ml probably derived from a non-platelet source, and plasma thrombospondin levels do not simply reflect platelet release.

Enhancement of ADP-induced Platelet Aggregation by Adrenaline in Vivo and Its Prevention

1973 ◽  
Vol 29 (02) ◽  
pp. 490-498 ◽  
Author(s):  
Hiroh Yamazaki ◽  
Itsuro Kobayashi ◽  
Tadahiro Sano ◽  
Takio Shimamoto
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
The Other ◽  
Endothelial Surface ◽  
Important Interaction ◽  
Blood Coagulability ◽  
The Difference

SummaryThe authors previously reported a transient decrease in adhesive platelet count and an enhancement of blood coagulability after administration of a small amount of adrenaline (0.1-1 µg per Kg, i. v.) in man and rabbit. In such circumstances, the sensitivity of platelets to aggregation induced by ADP was studied by an optical density method. Five minutes after i. v. injection of 1 µg per Kg of adrenaline in 10 rabbits, intensity of platelet aggregation increased to 115.1 ± 4.9% (mean ± S. E.) by 10∼5 molar, 121.8 ± 7.8% by 3 × 10-6 molar and 129.4 ± 12.8% of the value before the injection by 10”6 molar ADP. The difference was statistically significant (P<0.01-0.05). The above change was not observed in each group of rabbits injected with saline, 1 µg per Kg of 1-noradrenaline or 0.1 and 10 µg per Kg of adrenaline. Also, it was prevented by oral administration of 10 mg per Kg of phenoxybenzamine or propranolol or aspirin or pyridinolcarbamate 3 hours before the challenge. On the other hand, the enhancement of ADP-induced platelet aggregation was not observed in vitro, when 10-5 or 3 × 10-6 molar and 129.4 ± 12.8% of the value before 10∼6 molar ADP was added to citrated platelet rich plasma (CPRP) of rabbit after incubation at 37°C for 30 second with 0.01, 0.1, 1, 10 or 100 µg per ml of adrenaline or noradrenaline. These results suggest an important interaction between endothelial surface and platelets in connection with the enhancement of ADP-induced platelet aggregation by adrenaline in vivo.

The Effects of Brinolase (Fibrinolytic Enzyme from Aspergillus Oryzae) on Platelet Aggregation of Dog and Man

1972 ◽  
Vol 28 (01) ◽  
pp. 031-048 ◽  
Author(s):  
W. H. E Roschlau ◽  
R Gage
Keyword(s):  
Platelet Aggregation ◽  
Aspergillus Oryzae ◽  
Degradation Products ◽  
Blood Platelet ◽  
Human Platelets ◽  
Fibrinolytic Enzyme ◽  
Inhibitory Effects ◽  
Blood Platelet Aggregation

SummaryInhibition of blood platelet aggregation by brinolase (fibrinolytic enzyme from Aspergillus oryzae) has been demonstrated with human platelets in vitro and with dog platelets in vivo and in vitro, using both ADP and collagen as aggregating stimuli. It is suggested that the optimal inhibitory effects of brinolase occur indirectly through the generation of plasma fibrinogen degradation products, without compromising platelet viability, rather than by direct proteolysis of platelet structures.

Release, Aggregation and Lysis of Human Platelets by Antilymphocyte Globulin and Antiplatelet Serum

1976 ◽  
Vol 36 (02) ◽  
pp. 411-423 ◽  
Author(s):  
Nicholas Lekas ◽  
J. C Rosenberg
Keyword(s):  
Platelet Aggregation ◽  
Gamma Globulin ◽  
Human Platelets ◽  
Plasma Medium ◽  
Release Reaction ◽  
Clinical Events ◽  
Thrombotic Complications ◽  
Platelet Release ◽  
Free Media

SummaryHuman platelets labeled with 51Cr were used to determine the contribution made by platelet lysis to the platelet release reaction and platelet aggregation induced by rabbit antihuman platelet serum (APS) and equine antihuman thymocyte globulin (ATG). Platelets were tested in both plasma (PRP) and non-plasma containing media. Antibodies directed against platelets, either as APS or ATG, induced significant amounts of platelet release and aggregation, as well as some degree of lysis, in the absence of complement. The presence of complement increased platelet lysis and aggregation, but not the release reaction. Non-immune horse gamma globulin produced different responses depending upon whether platelets were investigated in PRP or non-plasma containing media. Aggregation was seen in the latter but not the former. These differences can be explained by the presence of plasma components which prevent non-specific immune complexes from causing platelet aggregation. Since platelets in vivo are always in a plasma medium, one must be wary of utilizing data from platelet studies in synthetic plasma-free media as the basis of explaining clinical events. These observations demonstrate at least two, and possibly three, different mechanisms whereby ATG could activate platelets causing thrombotic complications and thrombocytopenia, i.e., via 1) specific and, 2) non-specific non-lytic pathways and 3) a lytic pathway.

Platelet Aggregation in Whole Blood: The Role of Thromboxane A2 and Adenosine Diphosphate

1985 ◽  
Vol 54 (03) ◽  
pp. 612-616 ◽  
Author(s):  
A J Carter ◽  
S Heptinstall
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Adenosine Diphosphate ◽  
Blood Platelet ◽  
Thromboxane B2 ◽  
Lipoxygenase Inhibitor ◽  
Thromboxane Synthase Inhibitor ◽  
Synthase Inhibitor

SummaryThe platelet aggregation that occurred in whole blood in response to several aggregating agents (collagen, arachidonic acid, adenosine diphosphate, adrenaline and thrombin) was measured using an Ultra-Flo 100 Whole Blood Platelet Counter. The amounts of thromboxane B2 produced were measured by radioimmunoassay. The effects of various inhibitors of thromboxane synthesis and the effects of apyrase, an enzyme that destroys adenosine diphosphate, were determined.Platelet aggregation was always accompanied by the production of thromboxane B2, and the amounts produced depended on the nature and concentration of the aggregating agent used. The various inhibitors of thromboxane synthesis - aspirin and flurbiprofen (cyclo-oxygenase inhibitors), BW755C (a cyclo-oxygenase and lipoxygenase inhibitor) and dazoxiben (a selective thromboxane synthase inhibitor) - did not markedly inhibit aggregation. Results obtained using apyrase showed that adenosine diphosphate contributed to the aggregation process, and that its role must be acknowledged when devising means of inhibiting platelet aggregation in vivo.

scholarly journals Methods: Blood Platelet Counts of the Golden Hamster, Cricetus auratus

Blood ◽  
1952 ◽  
Vol 7 (9) ◽  
pp. 948-949 ◽  
Author(s):  
KENNETH OTTIS ◽  
OSCAR E. TAUBER
Keyword(s):  
Platelet Count ◽  
Adult Male ◽  
Golden Hamster ◽  
Healthy Adult ◽  
Blood Platelet ◽  
Male And Female ◽  
Platelet Counts ◽  
Healthy Adult Male ◽  
Blood Platelet Count ◽  
Direct Counts

Abstract Healthy, adult male and female golden hamsters, 3 months of age, showed blood platelet count means of 688,000 ± 141,000 per cu. mm. and 742,000 ± 120,000 per cu. mm., respectively, when direct counts were made with siliconized pipets and with Rees and Ecker fluid as a diluent.

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