Studies of Platelet Aggregation, Plasma Adenosine Diphosphate Breakdown and Blood Coagulation in Magnesium Deficient Calves and Rats

1970 ◽  
Vol 23 (02) ◽  
pp. 299-305 ◽  
Author(s):  
M. M Stevenson ◽  
I. I Yoder
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Serum Magnesium ◽  
Adenosine Diphosphate ◽  
Clinical Implications ◽  
Platelet Poor Plasma ◽  
Significant Difference ◽  
Procoagulant Effect ◽  
Plasma Adenosine

SummaryADP-induced platelet aggregation and the breakdown of ADP in platelet-poor plasma of normal and magnesium deficient calves and rats have been studied. There was no statistically significant difference in ADP-induced platelet aggregation between the treated and untreated groups of animals. There was a significant difference in the ADP breakdown in platelet poor plasma of magnesium deficient rats as compared to the untreated animals. The platelet count of the magnesium deficient calves and in the citrated platelet-rich plasma of the magnesium deficient rats was not different from the normal. The thrombin clotting and partial thromboplastin times were significantly shortened in the magnesium deficient calves, but the prothrombin time was not affected. These findings suggest that pathological alterations in the serum magnesium levels that are still compatible with life do not influence adenosine diphosphate-induced platelet aggregation but do affect the breakdown of adenosine diphosphate in the plasma of rats. Just as magnesium administration may produce an anticoagulant effect, so may magnesium depletion produce a procoagulant effect in the blood of animals rendered magnesium deficient by diet. The clinical implications of this are discussed.

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.

Second Phase Platelet Aggregation Induced by Adenosine Diphosphate in Patients with Cerebral Vascular Disease and in Control Subjects

1970 ◽  
Vol 23 (01) ◽  
pp. 159-169 ◽  
Author(s):  
G Danta
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Vascular Disease ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Second Phase ◽  
Cerebral Vascular Disease ◽  
The Mean ◽  
Phase Platelet ◽  
Cerebral Vascular

SummaryAdenosine diphosphate-induced second phase platelet aggregation was studied in 70 patients with established cerebral vascular disease, 27 patients with chronic cerebral vascular disease taking dipyridamole, and 53 control subjects. The appearances of aggregation graphs relating changes in optical density in platelet-rich plasma to time after addition of adenosine diphosphate are described. An intermediate rate change in optical density was observed between first and second phase aggregation.Induction of second phase aggregation depends on the concentration of adenosine diphosphate and the platelet count of the plasma. Individual rseponses vary greatly, and there is appreciable variability in repeated estimations, but in the same plasma responses to adenosine diphosphate are accurately reproducible.In both patients and controls the mean logarithm of the adenosine diphosphate concentration that just induces second phase aggregation is inversely proportional to the mean platelet count of platelet-rich plasma. At all platelet concentrations studied, the smallest concentration of adenosine diphosphate that brought about second phase aggregation was significantly less in the patients than in controls. There was no significant correlation between the means of the two variables in patients taking dipyridamole. The findings in this group of patients accord with the assumption that dipyridamole favourably affects the abnormal reaction of platelets to adenosine diphosphate in some of the patients with cerebral vascular disease.

scholarly journals Intraoperative collection of autologous platelet-rich plasma from the cardiopulmonary bypass circuit upon initiation of extracorporeal circulation

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Takeshi Honda ◽  
Yuji Kanaoka ◽  
Hiroshi Furukawa ◽  
Taishi Tamura ◽  
Noriaki Kuwada ◽  
...  
Keyword(s):  
Platelet Count ◽  
Cardiopulmonary Bypass ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Collection System ◽  
Blood Samples ◽  
Autologous Platelet Rich Plasma ◽  
The Mean ◽  
Autologous Platelet

Abstract Objectives The aim of this study is to evaluate the possibility of the autologous platelet-rich plasma (PRP) collection from the cardiopulmonary bypass (CPB) circuit and to evaluate its effect on the aggregative function. Methods For seventy-two patients undergoing cardiac surgery with CPB, an autologous PRP was prepared using the Haemonetics Component Collection System® by drawing blood from the CPB circuit immediately after CPB was established. The blood samples were taken at three points for examination, A: beginning of surgery, B: immediately after heparin reversal with protamine following discontinuation of CPB, C: after the collected autologous PRP was returned to the patient. Platelet count and platelet aggregation ability were analyzed. Results The mean platelet count in autologous PRP was 5.5 (range: 3–14) units. Platelet count decreased by 115.0 (±27.3) × 1000/μl from A to B and increased by 27.3 ± 17.2 (× 1000/μl) from B to C. When platelet aggregation was measured by Adenosine Diphosphate (ADP) 3.0 μM, it decreased by 42.6% ± 12.1% from A to B and increased by 8.7% ± 7.4% from B to C. Conclusions Autologous PRP can be safely collected by drawing blood from the CPB circuit, platelet count and aggregation ability significantly decreased after CPB including autologous PRP collection. Some improvement was detected in the number of the platelets count and platelet aggregation ability by administrating an autologous PRP even if autologous PRP is collected from CPB circuit. Trial registration UMI-CTR, UMIN000023776. Registered 1 October 2016.

Investigation of Platelet Functions in Chronic Myeloproliferative Disorders by Optical and Luminesance Method.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4766-4766
Author(s):  
Meltem O. Akay ◽  
Fezan S. Mutlu ◽  
Zafer Gulbas
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Reference Range ◽  
Platelet Rich Plasma ◽  
Atp Release ◽  
Adenosine Diphosphate ◽  
Myeloproliferative Disorders ◽  
Test Results ◽  
Chronic Myeloproliferative Disorders ◽  
Significant Difference

Abstract Background: Bleeding and thrombosis are common causes of morbidity and mortality in patients with myeloproliferative disorders (MPD). Qualitative platelet abnormalities are frequently found in these patients and range from platelet hypofunction as demonstrated by defective invitro platelet aggregation, acquired storage pool disease and/or platelet membrane defects, in addition to enhanced platelet aggregation, increased plasma beta thromboglobulin levels or shortened platelet survival. In this study we aimed to perform platelet aggregation studies by optical method (on platelet rich plasma=PRP) and luminesance method (on whole blood) in chronic myeloproliferative disorders. Methods:A total of twenty-five patients with MPD (17 chronic myeloid leukemia, 6 polycythemia vera, 2 essential thrombocytosis) were enrolled. Median age was 54,4 (29–76). Platelet aggregation was measured using the optic and luminesance method. The agonists used were adenosine diphosphate (ADP), arachidonic acid (AA) ristocetin and collagen. Platelets were considered to be hyperactive if at least one result (i.e. aggregation or ATP release with one agonist) was above the reference range, and hypoactive if at least one result (i.e. aggregation or ATP release) was below the reference range. Mixed hypo- and hyperactive platelets were considered present when at least one result (i.e. aggregation or ATP release) was below and above the reference range respectively. Results:Platelet aggregation test results by two methods in myeloproliferative disorders were shown in Table 1. The percent for detection of platelet function abnormality by luminesance method was found to be higher than the optic method and a significant difference was shown between two methods (p<0,05). Conclusion Our findings suggest that;1. Luminesance platelet aggregation study is more valuable than optic platelet aggregation study for invitro assessment of platelet function in patients with MPD. 2. The use of luminesance platelet aggregation study appears useful to select patients for antiplatelet therapy. Platelet aggregation test results in myeloproliferative disorders (n=25) Normal Hypofunction Hyperfunction Mix Total abnormality Luminesance method 1(%4) 4(%16) 8(%32) 11(%44) 24(%96) Optic method 9(%36) 11(%44) 2(%8) 3(%12) 16(%64)

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.

Stimulated Platelet Aggregation, Thromboxane B2 Formation and Platelet Sensitivity to Prostacyclin - A Critical Evaluation

1981 ◽  
Vol 45 (03) ◽  
pp. 204-207 ◽  
Author(s):  
Wolfgang Siess ◽  
Peter Roth ◽  
Peter C Weber
Keyword(s):  
Arachidonic Acid ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Reliable Method ◽  
Platelet Rich Plasma ◽  
Critical Evaluation ◽  
Vascular Diseases ◽  
Thromboxane B2 ◽  
Test Time ◽  
Stimulation Of

SummaryPlatelets have been implicated in the development of atherosclerotic and thrombotic vascular diseases. Evaluation of platelet aggregation in relation to endogenously formed compounds which affect platelet function may provide information of clinical and pharmacological relevance. We describe a method in which thromboxane B2 (TXB2) formation was analyzed following stimulation of platelet-rich plasma (PRP) with ADP, 1-epinephrine, collagen, and arachidonic acid. In addition, we determined platelet sensitivity to prostacyclin following ADP- and collagen-induced platelet aggregation. The parameters under study were found to depend on the platelet count in PRP, on the type and dose of the aggregating agent used, and on the test time after blood sampling. By standardization of these variables, a reliable method was established which can be used in clinical and pharmacological trials.

The Effect of Warfarin Sodium on the Duration of Platelet Aggregation

1967 ◽  
Vol 18 (03/04) ◽  
pp. 766-778 ◽  
Author(s):  
H. J Knieriem ◽  
A. B Chandler
Keyword(s):  
Platelet Count ◽  
Placebo Group ◽  
Platelet Aggregation ◽  
Prothrombin Time ◽  
Platelet Rich Plasma ◽  
Healthy Adults ◽  
Double Blind Study ◽  
Double Blind ◽  
Warfarin Sodium

SummaryThe effect of the administration of warfarin sodium (Coumadin®) on the duration of platelet aggregation in vitro was studied. Coumadin was given for 4 consecutive days to 10 healthy adults who were followed over a period of 9 days. The duration of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma, the prothrombin time, and the platelet count of platelet-rich plasma were measured. Four other healthy adults received placebos and participated in a double-blind study with those receiving Coumadin.Although administration of Coumadin caused a prolongation of the prothrombin time to 2 or 21/2 times the normal value, a decrease in the duration of platelet aggregation was not observed. In most individuals who received Coumadin an increase in the duration of platelet aggregation occurred. The effect of Coumadin on platelet aggregation was not consistently related to the prothrombin time or to the platelet count. In the placebo group there was a distinct relation between the duration of platelet aggregation and the platelet count in platelet-rich plasma.The mean increase in the duration of platelet aggregation when compared to the control value before medication with Coumadin was 37.7%. In the placebo group there was a mean increase of 8.4%. The difference between the two groups is significant (p <0.001). Increased duration of platelet aggregation also occurred in two individuals who received Coumadin over a period of 10 and 16 days respectively.

scholarly journals Influence of Hepatocellular Carcinoma on Platelet Aggregation in Cirrhosis

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1150
Author(s):  
Alberto Zanetto ◽  
Marco Senzolo ◽  
Elena Campello ◽  
Cristiana Bulato ◽  
Sabrina Gavasso ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Adenosine Diphosphate ◽  
Compensated Cirrhosis ◽  
Impedance Aggregometry ◽  
Child Class ◽  
Von Willebrand ◽  
Willebrand Factor

Hyper-functional platelets are being proposed as a potential therapeutic target in multiple cancers. Whether this can be considered in patients with cirrhosis and hepatocellular carcinoma (HCC) is unknown as their platelet function has not yet been investigated. We evaluated platelet function in cirrhosis patients with HCC. Patients with cirrhosis with and without HCC were prospectively recruited. Platelet aggregation, a marker of platelet function, was assessed by impedance aggregometry with adenosine diphosphate (ADP), arachidonic acid (ASPI), and thrombin (TRAP) stimulation. Plasmatic levels of Von Willebrand factor antigen (VWF) were also determined. One-hundred patients were recruited (50 cirrhotics with and 50 without HCC). Cirrhosis severity by Child class and platelet count were comparable between cirrhotics with and without HCC. Cirrhotics with HCC had higher ADP- (45 vs. 28; p < 0.001), ASPI- (47 vs. 28; p < 0.001), and TRAP- (85 vs. 75; p = 0.01) induced platelet aggregation than cirrhotics without HCC, all indicative of platelet hyper-function. The relatively increased platelet aggregation in patients with HCC was confirmed after adjusting the analysis for platelet count/severity of thrombocytopenia. Levels of VWF were higher in patients with vs. without HCC (348 vs. 267; p = 0.006), particularly in compensated cirrhosis. In patients with cirrhosis, HCC is associated with increased platelet aggregation and higher VWF. The clinical implications of these findings deserve further investigation.

WHOLE BLOOD AGGREGOMETER IN THE ASSESSMENT OF PLATELET HYPER-AGGREGABILITY

1987 ◽  
Author(s):  
R Abbate ◽  
M Boddi ◽  
S Favilla ◽  
G Costanzo ◽  
R Paniccia ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Vascular Complications ◽  
Thromboembolic Complications ◽  
Significant Difference ◽  
Platelet Number ◽  
Patient Groups ◽  
Clinical Conditions ◽  
Selection Of

The aim of this study has been to investigate the reliability of platelet aggregation in whole blood in some clinical conditions associated to thromboembolic complications.18 healthy subjects, 15 patients affected by ischemic heart disease (IHD) and 15 patients affected by insulin independent diabetes, free of vascular complications, were studied. Collagen induced (2.5 mg/L f.c.) platelet aggregation was evaluated both in whole blood (WB) by using impedance whole blood aggregometer (Chrono-Log) and in platelet rich plasma (PRP) by Born aggregometer. Aggregation was significantly higher in whole blood than in PRP in all the groups investigated (p < 0.01). No significant difference was found in PRP aggregation among the three groups, whereas WB aggregation was significantly higher in the two patient groups (IHD 79.5 + 14.2%, Diabetes 81.3 + 17.6%) than in controls (64.8 ± 14.1%) (p < 0.01 for both comparisons). No relationship was found between WB aggregation and Hct or platelet number in any of the groups studied. A slight relationship was found between megathrombocyte count and WE aggregation values (r=0.31, p < 0.05).Collagen platelet aggregation in WB seems to be provided with higher sensibility than PRP aggregation in detecting hyper-aggregability, probably because it does not imply the selection of platelet populations with loss of larger platelets and of other blood cells.

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