scholarly journals Platelet Counts Analysis of Platelet-Poor Plasma (PPP) Produced by Several Centrifugation Techniques

2020 ◽  
Keyword(s):  
Platelet Poor Plasma ◽  
Platelet Counts

Reduced Platelet Aggregation in Hemolytic-Uremic Syndrome

1980 ◽  
Vol 43 (02) ◽  
pp. 154-157 ◽  
Author(s):  
Bernard S Kaplan ◽  
Jack S C Fong
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Hemolytic Uremic Syndrome ◽  
Early Phase ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Platelet Poor Plasma ◽  
Platelet Counts ◽  
Uremic Syndrome

SummaryPlatelet aggregation was studied in three patients during the course of the hemolytic-uremic syndrome (HUS) when the platelet count was below 100,000/mm3 and after the platelet count had normalized. Platelet aggregation was examined in response to epinephrine, adenosine diphosphate (ADP) and collagen. Aggregation did not occur in response to epinephrine when the patients were thrombocytopenic but normal tracings were obtained when the platelet counts had returned to normal. In contrast, platelet-rich plasma from normal subjects diluted with platelet-poor plasma from patients to comparable platelet counts, showed normal aggregation responses. This study demonstrates that platelet aggregation is reduced in the early phase of the HUS.

Platelet Factor 3 Activity in Washed Platelets

1973 ◽  
Vol 30 (03) ◽  
pp. 557-566 ◽  
Author(s):  
S Renaud ◽  
P Gautheron ◽  
H Rosenstein
Keyword(s):  
Thin Layer ◽  
Thin Layer Chromatography ◽  
Platelet Rich Plasma ◽  
The Other ◽  
Slow Speed ◽  
Platelet Factor ◽  
Platelet Poor Plasma ◽  
Platelet Counts ◽  
Edta Solution ◽  
Layer Chromatography

SummaryPlatelets collected with an EDTA solution and simply washed in an incomplete Tyrode’s presented clotting times in the recalcification (man and rat) and the Stypven (rat) tests that were practically identical to those of the PRP when slow speed centrifugation was used (800 G in man, 1000 G in rat). This was demonstrated, in 6 pools of 5 rats each and in 6 men, by comparing the clotting activity of the citrated platelet-rich plasma to that of the platelets washed and resuspended in the citrated platelet-poor plasma, for platelet counts ranging from 1 × 105 to 10 × 105/mm3. In contrast, centrifugation of platelets at 3000 G markedly affected these clotting activities, as was shown in an additional study comprising 6 pools of 3 rats.Finally, the clotting activity of platelets totally disrupted by sonication appears to be identical quantitatively in both man and rats to that of the total phospholipids extracted from these platelets and separated from the other lipids by thin-layer chromatography and resuspended in plasma by sonication.

scholarly journals Abnormal Platelets in Fulminant Hepatic Failure

1977 ◽  
Author(s):  
M.J. Weston ◽  
M.H. Rubin ◽  
G. Bullock ◽  
J. Roberts ◽  
P.G. Langley ◽  
...  
Keyword(s):  
Platelet Function ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Hepatic Necrosis ◽  
Second Phase ◽  
Platelet Poor Plasma ◽  
Platelet Counts ◽  
Prolonged Bleeding

Because bleeding occurs in fulminant hepatic failure, platelet function was investigated. In 12 patients, platelet counts were slightly lower than in controls (197 and 255 × 10 9/1, p<0.05), platelet volumes were smaller (5.89 and 6.68 μ3, p<0.001) and bleeding times were double (15.9 and 7.6 minutes, p<0.001). Patients’ platelets required ten times more ADP than controls to reach second phase aggregation (21.4 and 2.2 × 10-6m, p<0.001). Abnormalities of aggregation correlated with the prolonged bleeding times. Patient platelet poor plasma (PPP) did not prevent aggregation reaching second phase in controls and PPP from controls did not facilitate second phase aggregation in patients platelets. These defects of platelet function in fulminant hepatic failure are related to the severity of hepatic necrosis as platelet function in 16 jaundiced but non comatose patients did not differ from controls. Abnormalities of platelet ultrastructure are presented in an accompanying abstract.

Building and Clinical Use of Activated Plasma Clotting Time Test and the Value of APCT on Predicting the Bleeding Due to Leukemia Chemotherapy-Induced Thrombocytopenia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3915-3915
Author(s):  
Bao-An Chen ◽  
Jin-Jin Li ◽  
Cheng-Yin Huang ◽  
Feng Gao ◽  
Jian Chen ◽  
...  
Keyword(s):  
Sodium Citrate ◽  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Clinical Use ◽  
Clotting Time ◽  
Platelet Suspension ◽  
Platelet Poor Plasma ◽  
Platelet Counts ◽  
Significant Difference ◽  
Time Test

Abstract Objective This study was aimed to determine the optimal concertration of C-PG in activated plasma clotting time (APCT) test and build the APCT test.To investigate the value of activated plasma clotting time test (APCT) on predicting the bleeding due to Leukemia chemotherapy-induced thrombocytopenia. Method We collected healthy blood donors’venous blood, prepared watched platelet suspension and platelet rich plasma in a normal way to which we add different concertrations of C-PG, then test expression of AnnexinV in the surface of activated platelet by FCM. Prepared platelet rich plasma and platelet poor plasma in a normal way to which we add different concertrations of C-PG, then count the plasma clotting time.Forty-one patients with leukemia chemotherapy, twenty-one patients with petechiae or epistaxis or gum bleeding and twenty patients without bleeding symptoms, were involved in the test. Drawed their venous blood and collected in 3.2% buffered sodium citrate(9:1), the platelet counts and APCT, PT, APTT, TT, Fig were assesed. Result Bleeding group’s APCT was obviously prolonged contrast to the non-bleeding group’s. Platelet counts and APCT of the bleeding group and the non-bleeding group were (7.2±2.9) ×109/L, (105.9±8.1)s and (23.0±12.2) ×109/L,(71.4±9.0)s respectively. There was significant difference between the two groups (P&lt;0.01). Using APCT≥90s as the cut-off point to predict the bleeding caused by chemotherapy-induced thrombocytopenia, the sensibility was 100%, and the specificity was 95.7%. Using platelet counts ≤15*109/L, the sensibility and the specificity was 95.2% and 69.0%. PT, APTT, TT, Fig of the bleeding group and the non-bleeding group were 11.7±1.1)S,(31.5±1.3)S,(11.1±1.2)S,(2.37±0.41)g/L and (12.1±0.8)S,(30.8±2.1)S,(10.7±0.9)S,(2.64±0.27)g/L respectively. The results of the two groups were all not significantly different (P&gt;0.05). Conclusion APCT is a good indication of predicting the bleeding due to leukemia chemotherapy -induced thrombocytopenia.

Abstract WP255: Rapid Coagulation Tests for Acute Ischemic Stroke

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Hyun-Wook Nah ◽  
Dae-Hyun Kim ◽  
Jae-Kwan Cha
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Oral Anticoagulants ◽  
Standard Condition ◽  
Standard Group ◽  
Stroke Patients ◽  
Platelet Poor Plasma ◽  
Platelet Counts ◽  
High Acceleration ◽  
Coagulation Tests

Background and objectives: The results of coagulation tests are important for the decision of thrombolysis in acute ischemic stroke patients who are taking oral anticoagulants. In coagulation tests, the preparation of blood specimens is a major bottleneck in the workflow. Clinical and Laboratory Standard Institute (CLSI) guidelines require that routine coagulation tests are performed with platelet-poor plasma (<10,000 platelets per microliter). We investigated whether high acceleration centrifugation can reduce the time of coagulation tests without breaking the guidelines. Methods: We compared the high acceleration centrifugation condition (3 minutes, 8000 rpm) with the standard centrifugation condition (15 minutes, 3000 rpm) in 32 patients. The pre- and post-centrifugation platelet counts were measured and compared between the groups. Results: Sixteen samples were centrifuged in high acceleration condition and another 16 samples in standard condition. The pre-centrifugation platelet counts were not different (median, 165,000 (interquartile range, 146,750-185,500) per microliter vs. 166,500 (128,000-193,250), p=0.675) between the groups. Although the post-centrifugation platelet counts were higher in the high acceleration group than the standard group (4,500 (2,250-6,000) vs. 1,000 (0-2,000), p<0.001), all the samples in the high acceleration group met the requirements of platelet-poor plasma. Using the high acceleration centrifugation method, the reporting time of coagulation tests decreased from 24 (23-25) to 12 (12-13.5) minutes. Conclusion: High acceleration centrifugation can reduce the time of coagulation tests for 12 minutes without breaking the guidelines. This method may help to shorten the door-to-needle time in acute ischemic stroke patients who are taking oral anticoagulants.

Ultrastructural investigations of MDL 19,660-induced effects on the canine platelet and megakaryocyte

1990 ◽  
Vol 48 (3) ◽  
pp. 374-375
Author(s):  
D.E. Loudy ◽  
J. Sprinkle-Cavallo ◽  
J.T. Yarrington ◽  
F.Y. Thompson ◽  
J.P. Gibson
Keyword(s):  
Antidepressant Drug ◽  
Beagle Dogs ◽  
Long Term Effects ◽  
Short Term ◽  
Platelet Counts ◽  
Toxicological Studies ◽  
Induced Aggregation ◽  
Internal Architecture

Previous short term toxicological studies of one to two weeks duration have demonstrated that MDL 19,660 (5-(4-chlorophenyl)-2,4-dihydro-2,4-dimethyl-3Hl, 2,4-triazole-3-thione), an antidepressant drug, causes a dose-related thrombocytopenia in dogs. Platelet counts started to decline after two days of dosing with 30 mg/kg/day and continued to decrease to their lowest levels by 5-7 days. The loss in platelets was primarily of the small discoid subpopulation. In vitro studies have also indicated that MDL 19,660: does not spontaneously aggregate canine platelets and has moderate antiaggregating properties by inhibiting ADP-induced aggregation. The objectives of the present investigation of MDL 19,660 were to evaluate ultrastructurally long term effects on platelet internal architecture and changes in subpopulations of platelets and megakaryocytes.Nine male and nine female beagle dogs were divided equally into three groups and were administered orally 0, 15, or 30 mg/kg/day of MDL 19,660 for three months. Compared to a control platelet range of 353,000- 452,000/μl, a doserelated thrombocytopenia reached a maximum severity of an average of 135,000/μl for the 15 mg/kg/day dogs after two weeks and 81,000/μl for the 30 mg/kg/day dogs after one week.

Iron Deficiency Increases Platelet Counts in Rats

2009 ◽  
Vol 47 (05) ◽  
Author(s):  
R Evstatiev ◽  
A Bukaty ◽  
S Kulnigg ◽  
L Teischinger ◽  
C Gasche
Keyword(s):  
Iron Deficiency ◽  
Platelet Counts

Platelet Mobilization Induced by PAF and Its Role in the Thrombocytosis Triggered by Adrenaline in Rats

1989 ◽  
Vol 62 (04) ◽  
pp. 1107-1111 ◽  
Author(s):  
Hugo C Castro-Faria-Neto ◽  
Patricia T Bozza ◽  
Marco A Martins ◽  
Paulo M F L Dias ◽  
Patricia M R Silva ◽  
...  
Keyword(s):  
Receptor Antagonists ◽  
Blood Samples ◽  
Platelet Counts ◽  
Platelet Number ◽  
Edta Solution ◽  
Web 2086 ◽  
Dependent Mechanism

SummaryThe injection of PAP (6 μg/kg, i. v.) induced, in rats, haemoconcentration accompanied by an increase in the platelet number, as attested by the counts of platelets in blood samples diluted in formalin-free EDTA solution. This increase was significant at 15 min, peaked from 1 to 4 h and returned to basal levels 24 h after the lipid administration. The release of platelets induced by PAP was inhibited dose-dependently by specific PAP receptor antagonists such as WEB 2086 (0.5-2 mg/kg), BN 52021 and 48740 RP (5-25 mg/kg). Furthermore, platelet mobilization was clearly impaired in splenectomized animals stimulated by PAP, whereas thrombocytopenia and haemoconcentration by the same stimulus were intact. It was also noted that a second injection of PAP, 24 h after the initial stimulation with the lipid, failed to induce an increase in platelet counts, indicating autodesensitization. Desensitization to PAP or pretreatment with PAP antagonists clearly prevented the increase in the platelet counts after stimulation by adrenaline (15 μg/kg). These findings suggest that, in rats, PAP can induce release of platelets by a spleen-dependent mechanism and that this lipid may be relevant to the thrombocytosis triggered by adrenaline.

The Glycosaminoglycan of Recombinant Human Soluble Thrombomodulin Affects Antithrombotic Activity in a Rat Model of Tissue Factor-Induced Disseminated Intravascular Coagulation

1992 ◽  
Vol 67 (03) ◽  
pp. 366-370 ◽  
Author(s):  
Katsuhiko Nawa ◽  
Teru Itani ◽  
Mayumi Ono ◽  
Katsu-ichi Sakano ◽  
Yasumasa Marumoto ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Disseminated Intravascular Coagulation ◽  
Rat Model ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Soluble Thrombomodulin ◽  
Intravascular Coagulation ◽  
Platelet Counts ◽  
Recombinant Human Soluble Thrombomodulin

SummaryPrevious studies on recombinant human soluble thrombomodulin (rsTM) from Chinese hamster ovary cells revealed that rsTM was expressed as two proteins that differed functionally in vitro due to the presence (rsTMp) or absence (rsTMa) of chondroitin-4-sulfate. The current study evaluates the in vivo behavior of rsTM in rats and in a rat model of tissue factor-induced disseminated intravascular coagulation (DIC). rsTMp was more potent than rsTMa for prolongation of the activated partial thromboplastin time (APTT) and their in vivo half-lives determined by ELISA were 20 min for rsTMp and 5.0 h for rsTMa. Injection of a tissue factor suspension (5 mg/kg) resulted in DIC as judged by decreased platelet counts and fibrinogen concentrations, prolonged APTT, and increased fibrin and fibrinogen degradation products (FDP) levels. A bolus injection of either rsTM (0.2 mg/kg) 1 min before induction of DIC essentially neutralized effects on platelets, fibrinogen, and FDP levels, and had only a moderate effect on APTT prolongation. The dose of anticoagulant to inhibit the drop in platelet counts by 50% (ED50) was 0.2 mg/kg rsTMa, 0.07 mg/kg rsTMp, and 7 U/ kg heparin. The effect of increasing concentrations of rsTM and heparin on bleeding times were compared in experiments involving incision of the rat tail. Doubling of the bleeding times occurred at 5 mg/kg rsTMa, 3 mg/kg rsTMp or 90 U/kg heparin. These values represent a 25-fold increase over the ED50 for rsTMa, 43-fold for rsTMp and 13-fold for heparin. These results suggest that rsTMp is a potent anticoagulant to inhibit the platelet reduction when injected prior to the induction of DIC in rats.

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