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.

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.

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.

Adenosine Diphosphate Breakdown by the Plasma of Different Species and by Human Whole Blood and White Cells

1967 ◽  
Vol 18 (03/04) ◽  
pp. 779-787 ◽  
Author(s):  
C. H Bolton ◽  
P. R Emmons
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Myocardial Infarctions ◽  
Breakdown Rate ◽  
Human Whole Blood ◽  
Platelet Poor Plasma ◽  
Aggregation Response

Summary1. The breakdown rate of ADP (200 µM/ml) by the platelet-poor plasma of the animals studied (human, rabbit, cat, sheep and rat) is consistent within a species and characteristic of that species.2. The breakdown rate of ADP is related directly to the B. M. R. of that species.3. The platelet aggregation response to ADP is extremely variable even within a species, and bears little, if any, relationship to ADP breakdown.4. The breakdown of ADP added to whole blood has been studied both in normal subjects and in patients with myocardial infarctions. The breakdown patterns were found to be identical.5. The ADP-ase activity of whole blood was localised almost entirely in the white cells.

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.

Montreal Platelet Syndrome (MPS):Ultrastructural, Biochemical And Functional Studies

1981 ◽  
Author(s):  
M M Frojmovie ◽  
J G Milton ◽  
S S Tang
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Shape Change ◽  
Protein Profile ◽  
Peripheral Blood Smear ◽  
Ionophore A23187 ◽  
Clot Retraction ◽  
Platelet Counts

MPS is characterized by autosomal dominant inheritance thrombocytopenia (5,000-120,000 μl-1), abnormally large platelets on peripheral blood smear, spontaneous aggregation (SA), normal clot retraction and thromboplastin formation, nypervolumetric shape change and normal amounts of plasma membrane. Here we describe further characteristics of MPS for 3 siblings /5 affected family members. The ultrastructural features of MPS platelets were normal except for the high frequency of giant granules. Platelet aggregation (PA) was studied in citrated platelet-rich plasma at platelet counts of 5,000-40,000 μl-1 and was quantitated microscopically from the decrease in single platelet count. PA could be increased over that due to SA alone by the addition of ADP, adrenalin, collagen, ionophore A23187, arachidonic acid and ristocetin, suggesting that the response to these agents may be normal. The ristocetin-induced increase in PA was completely blocked by an IgG specific for BSS. In contrast, over a 4 year period, thrombin (0.2 units/ml) either did not or only slightly increased PA over SA for 3/3 donors. However, MPS platelets pelleted from ACD-PRP and resuspended in Tyrodes’, pH 7.4 at a platelet count of ~ 200,000 μ1-1 showed a normal response to thrombin by aggregometry. Only one donor’s platelets had both reduced sialic acid and glycoprotein (G.P.) 1 reduction/abnormality with otherwise normal G.P. and protein profile, while the other 2 siblings’ platelets showed no such abnormalities. The above results indicate that biochemical variability exists for MPS platelets from different affected siblings. Moreover, our observations raise the possibility that platelet aggregation abnormalities in thrombobytopenic disorders (may be obscured by (1) preparation artefacts and/or (2) artificially increasing platelet counts for in vitro studies.

scholarly journals Platelet Adherence of Collagen: A Simple Reproducible Method

1977 ◽  
Author(s):  
M.J. Mant
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Experimental Conditions ◽  
Optimal Method ◽  
Collagen Concentration ◽  
Platelet Counts ◽  
Platelet Adherence ◽  
Before And After ◽  
Sample Testing

An optimal method for measuring platelet adherence to collagen should be simple, quantitative, reproducible, adaptable to varying experimental conditions and have no interfering platelet aggregation nor use reagents potentially influencing the results. An adaptation of previously described techniques has been developed which satisfies most of these requirements. Platelets were stirred with a stable collagen suspension in 0.2% EDTA at 37°C. Platelet counts were performed with a Coulter counter before and after stirring and %. adherent platelets calculated. Platelet aggregation was excluded by phase contrast microscopy and by unchanged adherence after addition of aggregating agents (ADP and adrenalin) and an inhibitor of aggregation (prostaglandin El). The counting technique was validated by absence of particle counts with collagen alone and by simultaneous “manual” post-adherence platelet counts. Adherence % was found to plateau at a maximum value with time, increasing collagen concentration and increasing stirring speed. It fell exponentially with increasing platelet count and linearly when pH was reduced. Utilizing platelet rich plasma (PRP) at a platelet count of 300,000/μl, a final collagen concentration approximating 0.05 mg/ml, a stir speed of 900 rpm and a pH of 7 ± 0.5 adherence % on 30 normal donors varied from 43.0 to 59.3%. A normal range of 51.6 ± 8.2% (± 2 SD) was established. Replicate single sample testing gave a mean ± 2 SD of 51.9 ± 2.8%. Serial adhérences in 1 individual showed only minimal weekly variation. This simple, reproducible, quantitative method can be adapted to a wide variety of experimental conditions. It should therefore be useful for investigating many aspects of platelet adherence to collagen.

scholarly journals Eculizumab Therapy Leads to Rapid Resolution of Thrombocytopenia in Atypical Hemolytic Uremic Syndrome

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Han-Mou Tsai ◽  
Elizabeth Kuo
Keyword(s):  
Renal Function ◽  
Platelet Count ◽  
Hemolytic Uremic Syndrome ◽  
Plasma Exchange ◽  
Complement Activation ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Steady Increase ◽  
Platelet Counts ◽  
Plasma Exchange Therapy ◽  
Uremic Syndrome

Eculizumab is highly effective in controlling complement activation in patients with the atypical hemolytic uremic syndrome (aHUS). However, the course of responses to the treatment is not well understood. We reviewed the responses to eculizumab therapy for aHUS. The results show that, in patients with aHUS, eculizumab therapy, when not accompanied with concurrent plasma exchange therapy, led to steady increase in the platelet count and improvement in extra-renal complications within 3 days. By day 7, the platelet count was normal in 15 of 17 cases. The resolution of hemolytic anemia and improvement in renal function were less predictable and were not apparent for weeks to months in two patients. The swift response in the platelet counts was only observed in one of five cases who received concurrent plasma exchange therapy and was not observed in a case of TMA due to gemcitabine/carboplatin. In summary, eculizumab leads to rapid increase in the platelet counts and resolution of extrarenal symptoms in patients with aHUS. Concurrent plasma exchange greatly impedes the response of aHUS to eculizumab therapy. Eculizumab is ineffective for gemcitabine/carboplatin associated TMA.

Circulating “Empty” Platelets In Hemolytic Uremic Syndrome And Thrombotic Thrombocytopenic Purpura

1981 ◽  
Author(s):  
G Lüchters ◽  
U Budde ◽  
U Klehr ◽  
N Müller
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Hemolytic Uremic Syndrome ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Thrombocytopenic Purpura ◽  
Atp Secretion ◽  
Uremic Syndrome ◽  
Platelet Spreading ◽  
Induced Aggregation ◽  
Small Aggregation

In two patients (1 male, 1 female) the diagnosis of hemolytic uremic syndrome (HUS) and in one male patient the diagnosis of thrombotic thrombocytopenic purpura (TTP) was confirmed. All patients showed a platelet aggregating factor in plasma. PgI2-stimulating activity of patient’s plasma was defective or absent. Platelet count was low and platelet aggregation was severely impaired. Even with high amounts of ADP (20 μM) only first phase aggregation could be seen. Epinephrine induced aggregation was absent. The highest amount of collagen used (20 μg/ml) induced only a small aggregation and no ATP-secretion. Thrombin stimulated ATP-secretion was decreased while Ristocetin induced aggregation was normal. ATP- and ADP-content of platelets was low and ATP/ADP ratio was raised above the normal value. Platelet spreading was severely impaired.From these findings we conclude that at least part of the platelets in these related diseases are circulating “empty” platelets which underwent degranulation in the patient’s blood vessels.

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.

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