The Effect of Calcium and Magnesium on Rabbit Blood Platelet Aggregation in Vitro

1964 ◽  
Vol 12 (01) ◽  
pp. 179-200 ◽  
Author(s):  
Torstein Hovig
Keyword(s):  
Platelet Aggregation ◽  
Cation Exchange ◽  
Calcium Concentration ◽  
Blood Platelets ◽  
Blood Platelet ◽  
Rabbit Blood ◽  
Calcium And Magnesium ◽  
Induced Aggregation ◽  
Blood Platelet Aggregation

SummaryThe effect of calcium and magnesium on the aggregation of rabbit blood platelets in vitro was studied, with the following results:1. Platelet aggregation induced by ADP or collagen could be prevented by EGTA or EDTA. The aggregating effect was restored by recalcification. The effect was also restored by addition of magnesium in EDTA-PRP, but not in EGTA-PRP unless a surplus of calcium was present.2. Calcium remained in concentrations of the order of 0.15–0.25 mM after dialysis or cation exchange of plasma. Aggregation of washed platelets resuspended in such plasma could not be produced with ADP or collagen, unless the calcium concentration was increased or that magnesium was added.3. The adhesiveness of blood platelets to collagen was reduced in EGTA-PRP and EDTA-PRP. Release of ADP from platelets influenced by collagen could not be demonstrated either in EGTA-PRP (presence of magnesium) or in EDTA-PRP.4. It is concluded that calcium is a necessary factor both for the reaction leading to release of ADP and for the the aggregation produced by ADP.5. Thrombin induced aggregation of washed platelets suspended in tris-buffered saline in the presence of calcium. No effect of magnesium could be observed unless small quantities of calcium were present.

Release of a Platelet-Aggregating Substance (Adenosine Diphosphate) from Rabbit Blood Platelets Induced by Saline “Extract” of Tendons

1963 ◽  
Vol 09 (02) ◽  
pp. 264-278 ◽  
Author(s):  
Torstein Hovig
Keyword(s):  
Platelet Aggregation ◽  
Blood Platelets ◽  
Adenosine Diphosphate ◽  
Blood Platelet ◽  
Saline Extract ◽  
Rabbit Blood ◽  
Blood Platelet Aggregation

Summary1. Blood platelet aggregation was induced by addition of saline “extract” of tendons to citrated PRP (aggregation time 50—60 seconds). The aggregates were sedimented by centrifugation, and aggregating activity was demonstrated in the supernatant (termed supernat. A) with an aggregation time of about 15 seconds.2. It was demonstrated that the activity of the supernatant was due to ADP released from the platelets.3. The conclusion is drawn that the aggregation reaction initiated by the tendon “extract” can be divided into two steps: 1. release of ADP from the platelets, 2. aggregation caused by released ADP.4. The observations are discussed in relation to the formation of platelet plugs in vivo.

The Effects of Brinolase (Fibrinolytic Enzyme from Aspergillus Oryzae) on Platelet Aggregation of Dog and Man

1972 ◽  
Vol 28 (01) ◽  
pp. 031-048 ◽  
Author(s):  
W. H. E Roschlau ◽  
R Gage
Keyword(s):  
Platelet Aggregation ◽  
Aspergillus Oryzae ◽  
Degradation Products ◽  
Blood Platelet ◽  
Human Platelets ◽  
Fibrinolytic Enzyme ◽  
Inhibitory Effects ◽  
Blood Platelet Aggregation

SummaryInhibition of blood platelet aggregation by brinolase (fibrinolytic enzyme from Aspergillus oryzae) has been demonstrated with human platelets in vitro and with dog platelets in vivo and in vitro, using both ADP and collagen as aggregating stimuli. It is suggested that the optimal inhibitory effects of brinolase occur indirectly through the generation of plasma fibrinogen degradation products, without compromising platelet viability, rather than by direct proteolysis of platelet structures.

Multiple electrode aggregometry: A new device to measure platelet aggregation in whole blood

2006 ◽  
Vol 96 (12) ◽  
pp. 781-788 ◽  
Author(s):  
Andreas Calatzis ◽  
Sandra Penz ◽  
Hajna Losonczy ◽  
Wolfgang Siess ◽  
Orsolya Tóth
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Blood Platelet ◽  
Platelet Inhibition ◽  
New Device ◽  
Platelet Aggregometry ◽  
Spontaneous Platelet Aggregation ◽  
Induced Aggregation ◽  
Blood Platelet Aggregation ◽  
Multiple Electrode

SummarySeveral methods are used to analyse platelet function in whole blood. A new device to measure whole blood platelet aggregation has been developed, called multiple electrode platelet aggregometry (MEA). Our aim was to evaluate MEA in comparison with the single platelet counting (SPC) method for the measurement of platelet aggregation and platelet inhibition by aspirin or apyrase in diluted whole blood. Platelet aggregation induced by different concentrations of ADP, collagen and TRAP-6 and platelet inhibition by apyrase or aspirin were determined in citrateor hirudin-anticoagulated blood by MEA and SPC. MEA indicated that spontaneous platelet aggregation was lower, and stimulated platelet aggregation was higher in hirudin- than citrate-anticoagulated blood. In hirudin-anticoagulated, but not citrate-anticoagulated blood, spontaneous platelet aggregation measured by MEA was inhibited by apyrase. For MEA compared with SPC the dose response-curves of agonist-induced platelet aggregation in citrate- and hirudin-blood showed similar EC50 values for TRAP, and higher EC50 values for ADP (non-significant) and collagen (p<0.05). MEA and the SPC method gave similar results concerning platelet-inhibition by apyrase and aspirin. MEA was more sensitive than SPC to the inhibitory effect of aspirin in collagen-induced aggregation. In conclusion, MEA is an easy, reproducible and sensitive method for measuring spontaneous and stimulated platelet aggregation, and evaluating antiplatelet drugs in diluted whole blood. The use of hirudin as an anticoagulant is preferable to the use of citrate. MEA is a promising technique for experimental and clinical applications.

scholarly journals Erythropoietin does not increase whole-blood platelet aggregation in vitro

1994 ◽  
Vol 9 (5) ◽  
pp. 556-558
Author(s):  
J. E. Taylor ◽  
J. J. F. Belch ◽  
I. S. Henderson ◽  
W. K. Stewart
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Blood Platelet ◽  
Blood Platelet Aggregation

Platelet Aggregation: Induction By Means Of a Complex Between Endotoxin and Copper (Cu2+)

1971 ◽  
Vol 49 (11) ◽  
pp. 1236-1244 ◽  
Author(s):  
A. F. Lewis ◽  
R. C. Dickson
Keyword(s):  
Platelet Aggregation ◽  
Clinical Significance ◽  
Blood Platelets ◽  
Adenosine Diphosphate ◽  
Bacterial Endotoxin ◽  
Cupric Ion ◽  
Rabbit Blood ◽  
Initial Stage ◽  
Induced Aggregation

The presence of a complex formed between bacterial endotoxin and cupric ion (Cu2+) causes mammalian (human, pig, and rabbit) blood platelets to aggregate in suspension. Complexes formed between endotoxin and Zn2+, Co2+, Ni2+, Mn2+, Fe3+, Ca2+, Mg2+, Ba2+, Al3+, Be2+, Pb2+, Cd2+, Ag+, or Hg2+ do not cause aggregation. The initial stage of the aggregation induced by the complex is not inhibited by inhibitors of adenosine diphosphate (ADP) or collagen induced aggregation, and is not accompanied by release of measureable amounts of serotonin or ADP. The potential clinical significance of the phenomenon is noted.

scholarly journals Whole-Blood Platelet Aggregation Predicts In Vitro and In Vivo Primary Hemostatic Function in the Elderly

1995 ◽  
Vol 15 (6) ◽  
pp. 748-753 ◽  
Author(s):  
Jonathan D. Emery ◽  
David W. Leifer ◽  
Glaci L. Moura ◽  
Patricia Southern ◽  
James H. Morrissey ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Blood Platelet ◽  
The Elderly ◽  
Blood Platelet Aggregation

Inhibition of whole blood platelet aggregation by nicardipine, and synergism with prostacyclin in-vitro

1986 ◽  
Vol 41 (4) ◽  
pp. 509-518 ◽  
Author(s):  
IA Greer ◽  
JJ Walker ◽  
M McLaren ◽  
AA Calder ◽  
CD Forbes
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Blood Platelet ◽  
Blood Platelet Aggregation

EFFECT OF COLLAGEN AND CITRATE ON HEPARIN-HEDIATED PLATELET ANTIAGGREGATORY ACTIVITY

1987 ◽  
Author(s):  
S R Saba ◽  
H I Saba ◽  
G A Morelli
Keyword(s):  
Platelet Aggregation ◽  
Inhibitory Activity ◽  
Whole Blood ◽  
Sodium Citrate ◽  
Blood Platelet ◽  
Inhibit Platelet Aggregation ◽  
Agonist Activity ◽  
Antiaggregatory Activity ◽  
Induced Aggregation ◽  
Blood Platelet Aggregation

Heparin has been reported to inhibit platelet aggregation. Our studies show that this activity is easily demonstrable in washed platelet systems, but fails to occur in citrated platelet-rich plasma (PRP) in the presence of a variety of agonists, except collagen. Studies were performed to answer the following questions: (1) Why does heparin inhibit the aggregation of washed platelets but not of citrated PRP, which is the system commonly used for platelet aggregation studies? (2) What is the effect of heparin on platelet aggregation occurring in whole blood, where it can be examined both with and without the presence of sodium citrate? (3) Why does heparin consistently inhibit the collagen-induced aggregation even in citrated PRP, while it fails to inhibit aggregation caused by other agonists? Results of the studies clearly demonstrated that heparin has the ability to directly react with sodium citrate, causing loss of its inhibitory activity on platelets. The antiaggregatory activity of heparin in the presence of collagen as the agonists appears to be directly related to the blocking of collagen’s agonist activity by heparin. Small concentrations of heparin which were unable to inhibit aggregation per se, effectively blocked the collagen agonist activity on platelet aggregation when heparin was directly added to collagen. Further studies showed that heparin, in a native whole blood platelet aggregation system (in the absence of any anticoagulant), exhibited significant inhibitory activity. This activity was lost when citrate was present in the whole blood preparation. These studies, therefore, indicate that failure of heparin to inhibit platelet aggregation in citrated PRP does not negate the importance of this inhibitory activity. Reactivity of heparin with sodium citrate renders citrated systems unsuitable for studying heparin's effect upon platelets. The whole blood platelet aggregation system without the presence of anticoagulants appears to be a more suitable system for the study of heparin and platelet aggregation, and is closer to the physiological system. Heparin exhibits marked inhibitory activity on platelet aggregation in this system, and this suggests it may be an important activity which deserves further attention.

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