Platelet Adhesion to Insolubilized Aggregating Agents

1975 ◽  
Author(s):  
D. L. Heene ◽  
G. Grotemeyer ◽  
F. R. Matthias ◽  
H. G. Lasch
Keyword(s):  
Platelet Count ◽  
Reaction Time ◽  
Venous Thrombosis ◽  
Platelet Adhesion ◽  
Platelet Reactivity ◽  
Platelet Rich Plasma ◽  
Arterial Occlusive Disease ◽  
Chemical Fixation ◽  
Thromboembolic Complications ◽  
Healthy Donors

Platelet aggregating substances, such as bovine fibrinogen (FG) and collagen (Col), were insolubilized by means of chemical fixation to CNBr-activated agarose. Platelets exposed to bovine FG-ag or Col-ag readily adhere and “aggregate” to these insolubilized agents. An assay system was designed which indicates the platelet reactivity towards FG-ag and Col-ag by means of the decrease of platelet count in platelet rich plasma after exposure to the agarose bound aggregating substance. After evaluation of the standard conditions concerning reaction time, amount of substrate and degree of disappearance of platelets for PRP from healthy donors (arbitrarily set to 100% ) the procedure was applied to clinical cases and revealed significant (p < 0.001) increase of platelet reactivity in patients with venous thrombosis (n = 11), arterial occlusive disease (n = 12), hyperlipemia (n = 26) and storke (n = 6). Mainly the FG-ag test was found to be suitable to detect hyperactivity (up to 300%) in cases with thromboembolic complications and to control the effect of ASA.

scholarly journals Rabbit Heart Valve Basement Membrane: Low Platelet Reactivity

Blood ◽  
1973 ◽  
Vol 41 (3) ◽  
pp. 359-367 ◽  
Author(s):  
Arcot D. Suresh ◽  
Michael B. Stemerman ◽  
Theodore H. Spaet
Keyword(s):  
Endothelial Cells ◽  
Basement Membrane ◽  
Heart Valves ◽  
Platelet Adhesion ◽  
Platelet Reactivity ◽  
Platelet Rich Plasma ◽  
Rabbit Heart ◽  
Electron Microscopic ◽  
Mechanical Methods ◽  
Microscopic Studies

Abstract Electron microscopic studies were performed on rabbit heart valves, and all four valves were found to be lined with a continuous basement membrane (BM). The valvular BM was liable to digestion by either trypsin or collagenase, but brief exposure to trypsin was suitable for desquamating endothelial cells, while leaving BM exposed and intact. Such preparations were used to determine their platelet reactivity with heparinized and citrated whole blood or with platelet-rich plasma. Although various conditions of exposure were used, including shaking and centrifugation, little or no platelet adhesion to the BM was observed. With similar conditions of exposure, preparations of collagen showed massive platelet adhesion accompanied by aggregation. This vascular BM was similarly nonreactive to platelets when endothelial cell removal was accomplished by mechanical methods. Rabbit valvular BM appears to be a poorly thrombogenic surface.

scholarly journals PLATELET RICH PLASMA PREPARATION PROTOCOLS: A PRELIMINARY STUDY

2016 ◽  
Vol 3 (2) ◽  
pp. 104
Author(s):  
Hans Kristian Nugraha ◽  
Meiti Muljanti ◽  
Yetti Hernaningsih ◽  
Jusak Nugraha
Keyword(s):  
Platelet Count ◽  
Platelet Rich Plasma ◽  
Clinical Pathology ◽  
Pathology Laboratory ◽  
Healthy Donors ◽  
Preliminary Study ◽  
Centrifugation Method ◽  
Blood Bag ◽  
Reliable Methods ◽  
Stored Blood

Currently, therapy with Platelet Rich Plasma (PRP) has been widely used and continues to grow for various clinical applications. Along with its development, there are various options in the method of obtaining PRP, either automatic or manual, while one of the most reliable methods according to the literature is a double centrifugation method. The purpose of this research is to produce anoptimization of the double centrifugation method. This study used experimental data obtained by conducting a research at the Clinical Pathology Laboratory of Dr. Soetomo Hospital, Surabaya. Experiments were conducted on stored blood obtained from the blood bag from Indonesian Red Crossand fresh blood from healthy donors with CPD anticoagulant. Results: PRP with optimum platelet count could be made with sufficient personal laboratory skills and amounted to 4.11 times with the platelet count of 1.152 million using 1300 rcf for 5 minutes for the first centrifugation, and 2300 rcf for 7 minutes for the second centrifugation.

scholarly journals Heparin-induced thrombocytopenia: confirmation of diagnosis with in vitro methods

Blood ◽  
1975 ◽  
Vol 45 (3) ◽  
pp. 395-401 ◽  
Author(s):  
JC Fratantoni ◽  
R Pollet ◽  
HR Gralnick
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Venous Thrombosis ◽  
Platelet Rich Plasma ◽  
Control Population ◽  
Immune Mechanism ◽  
Heparin Induced Thrombocytopenia ◽  
In Vitro Methods ◽  
Heparin Administration

Profound thrombocytopenia developed in a patient during treatment with heparin for venous thrombosis. The platelet count increased toward normal when heparin administration was stopped, but fell abruptly when the drug was again given. Platelet aggregation occurred when heparin was added to the patient's platelet-rich plasma, or to normal platelets plus the patient's serum. This serum also effected release of 3H- serotonin from normal platelets. This pattern of aggregation was clearly different from that occasionally caused by heparin in a control population. The data is consistent with an effect of heparin on platelets, possibly mediated by on immune mechanism.

A Modification of the Wu and Hoak Method for the Determination of Platelet Aggregates and Platelet Adhesion

1985 ◽  
Vol 53 (03) ◽  
pp. 381-385 ◽  
Author(s):  
Sudhir K Bowry ◽  
Colin R M Prentice ◽  
J M Courtney
Keyword(s):  
Platelet Adhesion ◽  
Platelet Rich Plasma ◽  
Blood Collection ◽  
Buffer System ◽  
Modified Method ◽  
Healthy Donors ◽  
Platelet Aggregate ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates

SummaryThe Wu and Hoak method for determining circulating platelet aggregates has poor reproducibility; problems have been reported with the composition of the buffer systems, haemolysis, the effects of blood collection technique and a divergence of the platelet aggregate ratio in blood for healthy donors from the theoretical value of 1. Our investigations suggest that the original technique is highly operator-dependent, especially the collection of blood and the method of counting platelets after centrifugation. We describe an improved modification of the Wu and Hoak technique; a new buffer system has been developed and the proportion of blood in the buffered EDTA and buffered EDTA- formalin solutions has been altered to obtain platelet rich plasma. The platelet aggregate ratio (PAR) by this modified method for healthy donors in two different studies was 0.97 ± 0.02 and 0.98 ± 0.01 respectively. Finally, the principle of Wu and Hoak was used to measure accurately platelet adhesion, without the role of platelet-platelet interactions (aggregation). Platelet adhesion and aggregation were then used to evaluate the thrombogenicity of various artificial surfaces, including silicone rubber and polytetra- fluoroethylene (PTFE) vascular grafts.

scholarly journals Heparin-induced thrombocytopenia: confirmation of diagnosis with in vitro methods

Blood ◽  
1975 ◽  
Vol 45 (3) ◽  
pp. 395-401 ◽  
Author(s):  
JC Fratantoni ◽  
R Pollet ◽  
HR Gralnick
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Venous Thrombosis ◽  
Platelet Rich Plasma ◽  
Control Population ◽  
Immune Mechanism ◽  
Heparin Induced Thrombocytopenia ◽  
In Vitro Methods ◽  
Heparin Administration

Abstract Profound thrombocytopenia developed in a patient during treatment with heparin for venous thrombosis. The platelet count increased toward normal when heparin administration was stopped, but fell abruptly when the drug was again given. Platelet aggregation occurred when heparin was added to the patient's platelet-rich plasma, or to normal platelets plus the patient's serum. This serum also effected release of 3H- serotonin from normal platelets. This pattern of aggregation was clearly different from that occasionally caused by heparin in a control population. The data is consistent with an effect of heparin on platelets, possibly mediated by on immune mechanism.

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.

Involvement of 5-Hydroxytryptamine in Platelet Aggregation In Vivo in Rats and Guinea Pigs

1989 ◽  
Vol 61 (03) ◽  
pp. 463-467 ◽  
Author(s):  
G M Smith
Keyword(s):  
Platelet Count ◽  
Guinea Pigs ◽  
Platelet Adhesion ◽  
Adenosine Diphosphate ◽  
Rate Of Return ◽  
Low Doses ◽  
Dose Dependent ◽  
Higher Doses ◽  
Rat Platelets

SummaryIn this study, 5-hydroxytryptamine (5-HT) caused a dose- dependent fall in the circulating platelet count suggesting that 5-HT receptors are activated in rat platelets to cause platelet adhesion and aggregation. When low doses of adenosine diphosphate (ADP) were simultaneously injected with 5-HT, there was a significant potentiation of the responses to ADR Ketanserin significantly reduced the potentiated responses. When higher doses of ADP were infused with bolus injections of 5-HT there was no potentiation and ketanserin did not reduce these responses. Ketanserin did not inhibit the collagen-induced fall in circulating platelet count, but did significantly increase the rate of return to the basal platelet count compared with control. 5-HT did not cause a fall in platelet count in guinea-pigs

Platelet Adhesiveness and Fibrinolysis after Recent Cerebro-Vascular Accidents and their Relationship with Subsequent Deep Venous Thrombosis of the Legs

1976 ◽  
Vol 36 (01) ◽  
pp. 127-132 ◽  
Author(s):  
C. P Warlow ◽  
J. A. N Rennie ◽  
D Ogston ◽  
A. S Douglas
Keyword(s):  
Platelet Count ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Plasminogen Activator ◽  
Fibrinogen Level ◽  
Plasma Fibrinogen ◽  
Platelet Adhesiveness ◽  
Plasma Fibrinogen Level ◽  
Vascular Accidents ◽  
Subsequent Rise

SummaryIn fifteen patients with a cerebro-vascular accident resulting in an acute hemiplegia there was a subsequent rise in the platelet count and plasma fibrinogen level. There were no significant alterations in platelet adhesiveness, plasminogen activator, plasminogen, FR-antigen and haematocrit. Patients diagnosed as developing deep venous thrombosis with the 125I-fibrinogen technique had a significantly lower platelet adhesiveness and plasminogen level than those who were not.

Macroaggregation of Platelets in Plasma, as Distinct from Microaggregation in Whole Blood (and Plasma), as Determined Using Optical Aggregometry and Platelet Counting respectively, is Specifically Impaired following Cardiopulmonary Bypass in Man

1994 ◽  
Vol 72 (04) ◽  
pp. 511-518 ◽  
Author(s):  
Valentine C Menys ◽  
Philip R Belcher ◽  
Mark I M Noble ◽  
Rhys D Evans ◽  
George E Drossos ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Platelet Count ◽  
Cardiopulmonary Bypass ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Interquartile Range ◽  
Contributory Factor ◽  
Platelet Aggregability ◽  
Aggregate Growth

SummaryWe determined changes in platelet aggregability following cardiopulmonary bypass, using optical aggregometry to assess macroaggregation in platelet-rich plasma (PRP), and platelet counting to assess microaggregation both in whole blood and PRP. Hirudin was used as the anticoagulant to maintain normocalcaemia.Microaggregation (%, median and interquartile range) in blood stirred with collagen (0.6 µg/ml) was only marginally impaired following bypass (91 [88, 93] at 10 min postbypass v 95 (92, 96] prebypass; n = 22), whereas macroaggregation (amplitude of response; cm) in PRP stirred with collagen (1.0µg/ml) was markedly impaired (9.5 [8.0, 10.8], n = 41 v 13.4 [12.7,14.3], n = 10; p <0.0001). However, in PRP, despite impairment of macroaggregation (9.1 [8.5, 10.1], n = 12), microaggregation was near-maximal (93 [91, 94]), as in whole blood stirred with collagen. In contrast, in aspirin-treated patients (n = 14), both collagen-induced microaggregation in whole blood (49 [47, 52]) and macroaggregation in PRP (5.1 [3.8, 6.6]) were more markedly impaired, compared with control (both p <0.001).Similarly, in PRP, macroaggregation with ristocetin (1.5 mg/ml) was also impaired following bypass (9.4 [7.2, 10.7], n = 38 v 12.4 [10.0, 13.4]; p <0.0002, n = 20), but as found with collagen, despite impairment of macroaggregation (7.2 [3.5,10.9], n = 12), microaggregation was again near-maximal (96 [93,97]). The response to ristocetin was more markedly impared after bypass in succinylated gelatin (Gelo-fusine) treated patients (5.6 [2.8, 8.6], n = 17; p <0.005 v control), whereas the response to collagen was little different (9.3 v 9.5). In contrast to findings with collagen in aspirin-treated patients, the response to ristocetin was little different to that in controls (8.0 v 8.3). Impairment of macroaggregation with collagen or ristocetin did not correlate with the duration of bypass or the platelet count, indicating that haemodilution is not a contributory factor.In conclusion: (1) Macroaggregation in PRP, as determined using optical aggregometry, is specifically impaired following bypass, and this probably reflects impairment of the build-up of small aggregates into larger aggregates. (2) Impairment of aggregate growth and consolidation could contribute to the haemostatic defect following cardiac surgery.

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.

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