scholarly journals The Increased Effectiveness of Platelet Concentrates Prepared in Acidified Plasma

Blood ◽  
1966 ◽  
Vol 27 (4) ◽  
pp. 449-459 ◽  
Author(s):  
FREDERICK A. FLATOW ◽  
EMIL J. FREIREICH

Abstract Platelet concentrates prepared in acidified plasma (pH 6.5-6.7) are superior to concentrates prepared by standard methods, and are 80-90 per cent as effective as platelet rich plasma (PRP). The use of excess citric acid to acidify plasma promotes resuspension of the concentrate by eliminating clumping, which is a major factor in the decreased effectiveness of standard concentrates. Analysis of posttransfusion recovery and survival of platelets reveals no evidence of platelet injury in an acid medium. Acidification of PRP inhibits the aggregation of platelets by adenosine diphosphate (ADP). The presence of endogenous ADP may be an important factor in clumping during standard concentrate preparation. A method of acidification of PRP using citric acid is described which allows preparation of an effective concentrate from fresh whole blood without subjecting the red cells to acid pH. Reconstitution of the acidified platelet poor plasma and its native red cells increases the citrate molarity by less than 6 per cent and results in minimal decrease in pH of the whole blood.

1980 ◽  
Vol 44 (01) ◽  
pp. 006-008 ◽  
Author(s):  
D Bergqvist ◽  
K-E Arfors

SummaryIn a model using an isolated rabbit mesenteric preparation microvessels were transected and the time until haemostatic plugs formed was registered. Perfusion of platelet rich plasma gave no haemostasis whereas whole blood did. Addition of chlorpromazine or adenosine to the whole blood significantly prolonged the time for haemostasis, and addition of ADP to the platelet rich plasma significantly shortened it. It is concluded that red cells are necessary for a normal haemostasis in this model, probably by a combination of a haemodynamic and ADP releasing effect.The fundamental role of platelets in haemostatic plug formation is unquestionable but there are still problems concerning the stimulus for this process to start. Three platelet aggregating substances have been discussed – thrombin, adenosine diphosphate (ADP) and collagen. Evidence speaking in favour of thrombin is, however, very minimal, and the discussion has to be focused on collagen and ADP. In an in vitro system using polyethylene tubings we have shown that "haemostasis" can be obtained without the presence of collagen but against these results can be argued that it is only another in vitro test for platelet aggregation (1).To be able to induce haemostasis in this model, however, the presence of red blood cells is necessary. To further study this problem we have developed a model where haemostatic plug formation can be studied in the isolated rabbit mesentery and we have briefly reported on this (2).Thus, it is possible to perfuse the vessels with whole blood as well as with platelet rich plasma (PRP) and different pharmacological agents of importance.


Transfusion ◽  
2003 ◽  
Vol 43 (12) ◽  
pp. 1723-1728 ◽  
Author(s):  
Maria L. Lozano ◽  
Elena Pérez-Ceballos ◽  
Jose Rivera ◽  
Dragica Paunovic ◽  
Maria J. Candela ◽  
...  

2014 ◽  
Vol 39 (4) ◽  
pp. 195
Author(s):  
GhadaM El-Gohary ◽  
AzzaS El-Danasoury ◽  
MahiraI El-Mogy ◽  
Amal Farouk ◽  
GhadaS Neseem

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 946-946 ◽  
Author(s):  
Sherrill J. Slichter ◽  
Doug Bolgiano ◽  
Jill Corson ◽  
Mary Kay Jones ◽  
Todd Christoffel ◽  
...  

Abstract Background: With the introduction of bacterial testing, extended storage of platelets is now possible as long as platelet viability is maintained. Although apheresis platelets have recently been licensed for seven days of storage, platelet concentrates are still only licensed for five days. We performed studies to determine the post-storage viability of platelets stored as concentrates. As yet, there are no established criteria for platelet viability that must be met at the end of storage. However, two different criteria for evaluating post-storage platelet viability have been suggested: compare the stored platelet results with each donor’s fresh platelet results; or establish a fixed platelet standard with an expected mean value along with the lower limit of the 95% confidence interval (lower 95% CI) of the mean. Methods: Forty-four normal volunteers donated a unit of whole blood, the whole blood was centrifuged to give platelet-rich plasma (PRP), and the PRP was then centrifuged to produce a platelet concentrate. The platelet concentrates were re-suspended and stored in either 100% plasma or in 20% plasma and 80% Plasmalyte (a platelet storage solution) for five to eight days in Terumo Teruflex bags. At the end of storage, a sample of blood was obtained from each volunteer to prepare fresh platelets to compare the results of a fresh platelet transfusion with the transfusion of the same volunteer’s stored platelets. The fresh and stored platelets were alternately radiolabeled with either 51Cr or 111In, re-injected into their volunteer donor, and serial blood samples were drawn from the volunteer after transfusion of the fresh and stored platelets to determine platelet recoveries and survivals. Results: Results are shown in Table 1. Conclusions: After seven days of storage in plasma, the platelets could qualify for standards of: 74% and 53% as a simple ratio of fresh to stored platelet recoveries and survivals, respectively; according to Dumont’s method of analysis (Transfusion, in press), achievable stored platelet recoveries would be 63% of fresh and survivals would be 40% of fresh; and as a fixed standard, platelet recoveries averaged 45% and survivals 4.4 days with lower 95% CI’s of 35% and 3.3 days, respectively. After eight days of storage in plasma, platelet recoveries and survivals gave unacceptable results. Instead of increasing or at least maintaining post-storage platelet viability, Plasmalyte markedly reduced platelet viability compared to plasma stored platelets at each storage interval. In Vivo Radiolabeled Autologous Platelet Recoveries and Survivals STORAGE CONDITIONS PLATELET RECOVERIES (%) PLATELET SURVIVALS (Days) Solution Time (Days) N Fresh Stored Fresh Stored Data are given as the average ±1 S.D. Plasma 5 10 62±12 55±11 7.7±1.5 6.1±1.0 Plasma 6 10 61±7 46±12 8.2±1.5 5.1±1.6 Plasmalyte 6 3 47±30 29±16 5.1±3.4 1.8±0.2 Plasma 7 10 61±11 45±14 8.3±1.0 4.4±1.5 Plasmalyte 7 5 62±17 30±12 7.4±0.6 2.2±1.1 Plasma 8 3 67±12 31±8 8.3±0.6 2.9±0.8 Plasmalyte 8 3 70±3 21±8 8.2±0.8 0.7±0.1


Blood ◽  
1972 ◽  
Vol 40 (5) ◽  
pp. 688-696 ◽  
Author(s):  
Herman E. Kattlove ◽  
Benjamin Alexander ◽  
Frances White

Abstract Citrated platelet-rich plasma (PRP) was kept at cold temperatures or room temperature. After 4 hr or more at these temperatures, the PRPs were warmed 1 hr at 37°C. This prevents the spontaneous aggregation seen in chilled PRP that is stirred immediately after warming. Platelet aggregation in response to connective tissue (CT), epinephrine, and adenosine diphosphate (ADP) was considerably greater in the PRPs originally kept at cold temperatures. In addition, chilling would restore the aggregation of platelets whose function had deteriorated due to prolonged storage at warm temperatures. Neither ADP-induced refractoriness, serotonin uptake, or CT-induced serotonin release was affected by cold. Retention in glass bead columns was greater in platelets that had been chilled than in platelets kept at room temperature or 37°C. Thus, the storage of platelets at cold temperatures leads to changes that improve platelet aggregation but may also increase platelet adhesion, which would account for the decreased in vivo survival of platelets preserved for transfusion at cold temperatures.


1971 ◽  
Vol 26 (03) ◽  
pp. 455-466 ◽  
Author(s):  
R. B Davis ◽  
G. C Holtz

SummaryThe effects of lead on blood platelet function and ultrastructure have been investigated. Lead acetate was injected intravenously in 27 rats and was added to rat and human platelet rich plasma in vitro. In vitro studies showed that concentrations of 2.5 × 10-3 M lead acetate reduced or blocked aggregation of rat and human platelets by adenosine diphosphate, collagen, and thrombin. Radioactive serotonin release from human platelets was inhibited by 10-4 M lead acetate. One hour after the injection of lead, platelet aggregation by thrombin was reduced, but platelet aggregation by adenosine diphosphate and collagen showed little change. Three days after lead, aggregation of platelets by collagen and thrombin was blocked and aggregation by adenosine diphosphate reduced. Thrombocytopenia was present 4 days after intravenous lead acetate. Electron micrographs of platelets showed that the mean number of mitochondria per platelet was increased, whereas alpha granules were reduced. Dense bodies were not significantly changed. Lead acetate affects platelet function in concentrations reported in human bone marrow in lead poisoning, and may relate to the binding of free sulfhydryl groups by lead.


1982 ◽  
Vol 48 (03) ◽  
pp. 327-329 ◽  
Author(s):  
S C Fox ◽  
M Burgess-Wilson ◽  
S Heptinstall ◽  
J R A Mitchell

SummaryThe Ultra-Flo 100 Whole Blood Platelet Counter has proved a useful tool for measuring platelet aggregation in whole blood, the extent of aggregation being deduced from the number of single platelets that remain. The technique has allowed us to show that platelets aggregate spontaneously in citrated blood and in heparinized blood but not in whole blood collected into EDTA. The aggregation occurs during storage but its rate is enhanced by stirring and it occurs more readily when the whole blood has been exposed to plastic rather than glass. It occurs much more readily in whole blood from some individuals than from others and the process may involve adenosine diphosphate (ADP). The rate of aggregation in whole blood is enhanced by several aggregating agents including collagen, ADP and sodium arachidonate which are more usually studied in platelet-rich plasma.


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1153-1153
Author(s):  
Hobl Eva-Luise ◽  
Petra Jilma-Stohlawetz ◽  
Ulla Derhaschnig ◽  
Schoergenhofer Christian ◽  
Michael Schwameis ◽  
...  

Abstract Background Patients on anti-platelet therapy have a higher incidence of bleeding complications and reversal of anti-platelet drug effects is an important issue in emergency situations. For old and conventional anti-coagulants, reversal strategies are established. However, there is no experience or recommendation how to antagonize the reversible and highly effective P2Y12-inhibitor ticagrelor and how to restore platelet function following ticagrelor dosing. The aim of this study was to investigate an ex vivo model to reverse the effects of ticagrelor and to estimate the optimal quantity of platelet transfusions required to normalize platelet aggregation. Methods Healthy volunteers (n=20) ingested a loading dose of 180 mg ticagrelor. Blood samples were obtained at baseline to gain autologous platelet rich plasma and to perform aggregation studies after 3h, i.e. at the time of expected maximal ticagrelor concentrations and maximimal platelet inhibition. To normalize platelet aggregation, increasing amounts of autologous platelet rich plasma (PRP) were added ex vivo to hirudin anti-coagulated blood, by spiking PRP into blood at ratios of 1:10, 1:5 and 1:3. Platelet aggregation was assessed by whole blood multiple electrode aggregometry (MEA; Multiplate). For interpretation of aggregation, we defined a cutoff level of 40 U (Units) as the lower limit of the normal range. Volunteers above this level were considered to exhibit normal platelet reactivity. Nonparametric tests were used and statistical comparisons were performed with the Friedman ANOVA, and the Wilcoxon test for post-hoc comparisons. A two-tailed p-value of less than 0.05 was considered significant. Results Ingestion of 180 mg ticagrelor reduced average aggregation responses from 71 to 16 A.U. (p<0.001) and the platelet reactivity index in the VASP-assay from 88 to 22 units (p<0.001) A clear dose-response was obtained after spiking whole blood with increasing amounts of PRP. After addition of PRP at a ratio of 1:10, platelet aggregation increased to 31±14 U. When assuming that one apheresis platelet concentrate (200 mL) typically contains a minimum of 2 x1011 platelets, the ratio of 1:10 corresponds to 0.5 units of apheresis platelet concentrates. A ratio of 1:5 – equivalent to 1 unit of platelet concentrates – increased ADP induced platelet aggregation to 41±14 U. Platelet aggregation increased further to 48±18 U following the addition of PRP at a ratio of 1:3, which corresponds to 1.5 units of platelet concentrates (figure 1). All comparisons were significant at p<0.01. Conclusion Platelets dose-dependently improved ex vivo platelet aggregation of subjects after a loading dose of 180 mg of ticagrelor. It is estimated that > 2 units of apheresis platelet concentrates will be necessary to completely restore baseline platelet aggregation in the majority of patients. Point-of-care platelet function tests may be suitable tools to verify this concept in emergency patients and to estimate the extent of the reversal and de-risk on an individual patient’s level. Disclosures: No relevant conflicts of interest to declare.


Medicina ◽  
2009 ◽  
Vol 45 (9) ◽  
pp. 706 ◽  
Author(s):  
Vilma Kozlovaitė ◽  
Pranas Grybauskas ◽  
Jūratė Cimbolaitytė ◽  
Aušra Mongirdienė ◽  
Vytautas Šileikis ◽  
...  

Objective. To determine an influence of radiofrequency ablation on changes in coagulation system. Material and methods. We investigated 30 patients with cardiac arrhythmias. Platelet aggregation, fibrinogen and D-dimer level were analyzed before, right after, 24 and 72 h after radiofrequency ablation. Platelet aggregation was explored in whole blood and platelet-rich plasma using adenosine diphosphate (ADP), epinephrine, and collagen for induction. Results. Platelet aggregation induced by ADP and collagen in whole blood plasma increased significantly (P<0.01) (by 45% and 43%, respectively) in 24 h after radiofrequency ablation and remained increased in 72 h after radiofrequency ablation (by 11% and 35%, respectively) (P<0.01) as compared with baseline results. Spontaneous aggregation of platelet-rich plasma as well as ADP- and collagen-induced platelet aggregation tended to decrease right after radiofrequency ablation. Epinephrine-induced platelet aggregation significantly decreased by 17.5% after radiofrequency ablation (P<0.01) and started to increase in 24 h after radiofrequency ablation. In 72 h after radiofrequency ablation, platelet aggregation induced by different agonists increased by 7–45% significantly (P<0.05), and values were higher than baseline ones. Fibrinogen level after radiofrequency ablation did not differ from that of the baseline (3.08±0.7 g/L), but D-dimer level increased significantly (from 0.39±0.3 to 1.29±2.4 mg/L, P<0.01). In 24 h after radiofrequency ablation, an increase in fibrinogen level and a decrease in D-dimer level were found. Fibrinogen level increased to 3.32±0.6 g/L significantly in 72 h after radiofrequency ablation (P<0.05). Meanwhile, D-dimer concentration decreased to 0.78±0.8 mg/L, but it was still significantly higher (P<0.05) than the baseline value. Conclusion. Despite diminished platelet aggregation and increased D-dimer level right after radiofrequency ablation, a risk of thrombosis increased in the next few days after radiofrequency ablation.


1977 ◽  
Author(s):  
F. Schulte

Producing of a collagen preparation for determining platelet functions requires the testing of the activity of each single batch to make possible a standardization. For this purpose methods using PRP (platelet rich plasma) to measure the platelet aggregation are not very appropriate. Since four years a collagen centrifugation test proves to be suitable for determining the activity of various batches of Collagenreagent “Horm”. In this test the platelets of citrated whole blood are mixed with graduated doses of collagen directly by the withdrawal of blood. The turbidimetrical evaluation of the PRP obtained from the collagen treated whole blood samples shows 15% (SD ± 3. 5 %) of the O.D. (optical density) of the PFP (platelet free plasma) after a dose of 1 meg and 80% (SD ± 2 %) after a dose of 2 meg collagen per ml whole blood. The aggregation of platelets in citrated whole blood simultaneously with graduated doses of collagen allows to standardize different batches of platelet specific collagen preparations.


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