Heparin Counteracts the Antiaggregating Effect of Prostacyclin by Potentiating Platelet Aggregation

1983 ◽  
Vol 49 (02) ◽  
pp. 081-083 ◽  
Author(s):  
Vittorio Bertelé ◽  
Maria Carla Roncaglioni ◽  
Maria Benedetta Donati ◽  
Giovanni de Gaetano
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Specific Interaction ◽  
Inhibitory Effect ◽  
Effective Inhibitor ◽  
Inhibitory Potency ◽  
Human Platelet Aggregation

SummaryIt has recently been reported that heparin neutralizes the inhibitory effect of prostacyclin (PGI2) on human platelet aggregation. The mechanism of this interaction has not yet been unequivocally established. We present here evidence that heparin (Liquemin Roche) does not react directly with PGI2 but counteracts its inhibitory effect by potentiating platelet aggregation. In the absence of heparin, PGI2 was a less effective inhibitor of platelet aggregation induced by the combination of ADP and serotonin than by ADP alone. Moreover, the inhibitory effect of PGI2 was similarly reduced when increasing the concentrations of ADP (in the absence of heparin). The lack of a specific interaction between heparin and PGI2 is supported by the observation that, in the presence of heparin, other prostaglandins such as PGD2 and PGE1, and a non-prostanoid compound such as adenosine also appeared to lose their inhibitory potency. It is concluded that heparin opposes platelet aggregation inhibitory effect of PGI2 by enhancement of platelet aggregation.

Inhibitory Effect of Staphylokinase on Platelet Aggregation

1993 ◽  
Vol 70 (05) ◽  
pp. 834-837 ◽  
Author(s):  
Akira Suehiro ◽  
Yoshio Oura ◽  
Motoo Ueda ◽  
Eizo Kakishita
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Degradation Products ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Effective Concentration ◽  
Inhibit Platelet Aggregation ◽  
Platelet Suspension ◽  
Washed Platelet ◽  
Human Platelet Aggregation

SummaryWe investigated the effect of staphylokinase (SAK), which has specific thrombolytic properties, on human platelet aggregation. Platelet aggregation induced with collagen was observed following preincubation of platelets in platelet-rich plasma (PRP) or washed platelet suspension (WP) with SAK at 37° C for 30 min. SAK inhibited platelet aggregation in PRP only at the highest examined concentration (1 x 10-4 g/ml). Although SAK did not inhibit platelet aggregation in WP which contained fibrinogen, it did when the platelets had been preincubated with SAK and plasminogen. The most effective concentration in WP was 1 x 10-6 g/ml. The effect could be inhibited by adding aprotinin or α2-antiplasmin. The highest generation of plasmin in the same preincubation fluid was detected at 1 x 10-6 g/ml SAK. We concluded that SAK can inhibit platelet aggregation in WP by generating plasmin and/or fibrinogen degradation products, but is only partially effective in PRP because of the existence of α2-antiplasmin.

Potentiation of Adrenaline-Induced Platelet Aggregation by Angiotensin II

1985 ◽  
Vol 54 (03) ◽  
pp. 717-720 ◽  
Author(s):  
Yu-An Ding ◽  
D Euan MacIntyre ◽  
Christopher J Kenyon ◽  
Peter F Semple
Keyword(s):  
Platelet Aggregation ◽  
Angiotensin Ii ◽  
Human Platelet ◽  
Inhibitory Effect ◽  
Facilitatory Effect ◽  
Ang Ii ◽  
Human Platelet Aggregation ◽  
Low Concentrations ◽  
High Concentrations ◽  
Stimulation Of

SummaryThe effects of angiotensin II (ANG II) alone and in combination with other agonists on human platelet aggregation, thromboxane B2 (TxB2) and cytosolic [Ca2+]i were investigated. ANG II (10™11 - 10™7 M) alone had no direct effect on aggregation, TxB2 production or [Ca2+]i after short- (<2 min) or longterm (30 min) incubation. In contrast, low concentrations of ANG II (10™11 M) enhanced adrenaline-induced platelet aggregation but high concentrations (10™7 M) had an inhibitory effect. Moreover, ANG II (10™11 - 10™7 M) augmented platelet responses to the TxA2 mimetic, U44069. Pretreatment of platelets with flurbiprofen abolished this facilitatory effect of ANG II on adrenaline- but not on U44069-induced platelet aggregation. These results suggest that ANG II stimulation of agonist-induced platelet activation may be due to potentiation of the effects rather than the synthesis of TxA2

scholarly journals Inhibitory Effect of Hexahydrocurcumin on Human Platelet Aggregation

2012 ◽  
Vol 7 (7) ◽  
pp. 1934578X1200700 ◽  
Author(s):  
Huei-Ping Dong ◽  
Rei-Cheng Yang ◽  
I-Chun Chunag ◽  
Li-Ju Huang ◽  
Hsing-Tan Li ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Human Platelet Aggregation

The effects of hexahydrocurcumin on adenosine diphosphate (ADP)-induced human platelet aggregation were studied. Treatment of human platelet-rich plasma with hexahydrocurcumin resulted in an inhibitory effect on platelet aggregation, suggesting the potential of this compound as an anti-atherosclerogenic agent in humans.

Direct Inhibitory Mechanisms of Halothane on Human Platelet Aggregation

1996 ◽  
Vol 85 (1) ◽  
pp. 96-106 ◽  
Author(s):  
Shinji Kohro ◽  
Michiaki Yamakage
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Adenosine Monophosphate ◽  
Inhibitory Effect ◽  
Surface Glycoprotein ◽  
Dependent Manner ◽  
Glycoprotein Ib ◽  
Platelet Surface ◽  
Human Platelet Aggregation ◽  
Inhibitory Mechanisms

Background Although halothane directly inhibits platelet aggregation, the mechanisms of this effect are still unknown. The current study aimed to clarify the inhibitory mechanisms of halothane on thrombin-induced human platelet aggregation by measuring (1) platelet-surface glycoprotein Ib expression, (2) the concentration of intracellular free Ca2+ ([Ca2+]i) measured simultaneously with aggregation, (3) the concentration of intracellular inositol 1,4,5-triphosphate, and (4) the concentration of intracellular cyclic 3',5'-adenosine monophosphate ([cAMP]i). Methods Washed platelet suspensions, obtained from healthy volunteers, were preincubated with halothane (0-2 mM) for 2 min and then exposed to 0.02 units/ml thrombin for 3 min. The glycoprotein Ib bound to fluorescein-labeled antibody was measured by fluorescence flow cytometry. [Ca2+]i was measured, simultaneously with aggregation, in Fura-2 (Ca2+ indicator)-loaded platelets by use of a fluorometer. Inositol 1,4,5-triphosphate and [cAMP]i were measured by radioimmunoassay. Results Halothane had no effect on glycoprotein Ib expression with or without thrombin. Halothane decreased the thrombin stimulated [Ca2+]i transient and inhibited platelet aggregation in a dose-dependent manner, both in the presence and in the absence of external Ca2+. Isoflurane had no apparent effect on either platelet aggregation or [Ca2+]i in the absence of external Ca2+. Halothane inhibited the increase in inositol 1,4,5-triphosphate induced by thrombin. Halothane moderately but significantly increased [cAMP]i, but the adenylate cyclase activator forskolin (which has the same inhibitory ability on aggregation as halothane) increased [cAMP]i to a much greater extent than did halothane. Conclusions Halothane inhibits thrombin-induced human platelet aggregation by decreasing [Ca2+]i without inhibiting agonist-receptor binding; the inhibitory effect of halothane on [Ca2+]i might be mediated by a decrease in inositol 1,4,5 triphosphate and in part by an increase in [cAMP]i.

Identification of Platelet Inhibitor Present in the Melon (Cucurbitacea Cucumis Melo)

1985 ◽  
Vol 53 (03) ◽  
pp. 312-313 ◽  
Author(s):  
Raul Altman ◽  
Jorge Rouvier ◽  
Hans Weisenberger
Keyword(s):  
Platelet Aggregation ◽  
Mass Spectroscopy ◽  
Active Substance ◽  
Cucumis Melo ◽  
Human Platelet ◽  
Inhibitory Effect ◽  
Active Fraction ◽  
Uv Spectrum ◽  
Platelet Inhibitor ◽  
Human Platelet Aggregation

SummaryAn active fraction was isolated from an aqueous melon extract (Cucurbitacea cucumis melo) and was shown that it inhibits human platelet aggregation induced by epinephrine, ADP, collagen, thrombin, sodium arachidonate, prostaglandin endoperoxide analogue U-46619 and PAF-acether. Identification of the active substance as adenosine was indicated by TLC which gave identical Rf value compared to adenosine, by the UV spectrum, because the inhibitory effect on platelet aggregation disappeared after the addition of adenosine-deaminase and because the substance under study and adenosine produced the same spectra in the mass spectroscopy.

Inhibitory effect on human platelet aggregation, antioxidant activity, and phytochemicals of Canna warszewiczii (A. Dietr) Nb. tanaka

2020 ◽  
Vol 12 (1) ◽  
pp. 47
Author(s):  
NguyenThi Van Anh ◽  
LeHong Luyen ◽  
VuThi Thom ◽  
LeThi Thanh Huong ◽  
DuongThi Ly Huong
Keyword(s):  
Antioxidant Activity ◽  
Platelet Aggregation ◽  
Human Platelet ◽  
Inhibitory Effect ◽  
Human Platelet Aggregation

5'-N-Ethylcarboxamidoadenosine (NECA) Is A Potent, Stereospecific Inhibitor Of Human Platelet Aggregation

1981 ◽  
Author(s):  
N J Cusack ◽  
S M O Hourani
Keyword(s):  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Human Platelet ◽  
Human Platelets ◽  
Inhibit Platelet Aggregation ◽  
Inhibitory Potency ◽  
Adenosine Receptor Antagonist ◽  
Human Platelet Aggregation ◽  
Potent Vasodilator

Adenosine is a vasodilator, and also inhibits platelet aggregation apparently by acting at an external membrane receptor to increase levels of platelet cyclic AMP. Certain analogues of adenosine retain activity as vasodilators, and also inhibit platelet aggregation by raising levels of platelet cyclic AMP. NECA is an extraordinarily potent vasodilator, so its effects on human platelet function were tested.NECA (1 μM) inhibited human platelet aggregation induced by ADP, 5-HT, thrombin and adrenaline mere powerfully than adenosine (1 μM). NECA, even at micrcmolar concentrations, was 5 to 10 times more potent than adenosine as an inhibitor of aggregation induced by ADP (5μM or 200μM) or adrenaline (200μM). NECA (Ka = 0.95μM) caused increases in levels of platelet cyclic AMP, which could be competitively inhibited by theophylline (Ki = 8μM), an adenosine receptor antagonist. However, here NECA was only about 1.3 times more potent than adenosine (Ka = 1.2μM). The effects of NECA, like those of adenosine, were completely stereospecific, the L enantiomer of NECA being inactive. NECA (10μM) did not prevent inhibition of PGE1-stimulated adenylate cyclase by ADP (5 μM).NECA is the most potent analogue of adenosine yet tested on human platelets, and is the first example of a 5' modification to retain significant inhibitory potency.

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