Superoxide Dismutase Cooperates with Prostacyclin to Inhibit Platelet Aggregation: a Comparative Study in Washed Platelets and Platelet Rich Plasma

1991 ◽  
Vol 65 (04) ◽  
pp. 421-424 ◽  
Author(s):  
Daniela Salvemini ◽  
Gilberto de Nucci ◽  
John R Vane

SummaryThe role of superoxide anions (O2 −) in human platelet aggregation in Krebs’ buffer or plasma was investigated. In indome thacin (10 μM)-treated washed platelets superoxide dismutase (SOD; 60 U/ml) or ferricytochrome c (FCC; 70 μM) inhibited platelet aggregation by thrombin but not that by collagen or ADP. In addition, in indomethacin (10 μM)-treated washed platelets, SOD significantly potentiated the anti-aggregatory activity of prostacyclin (PGI2) or iloprost when thrombin but not collagen was used as the aggregating agent. In platelet rich plasma, SOD (60 U/ml) did not inhibit platelet aggregation nor did it potentiate the anti-aggregatory activity of iloprost when ADP, collagen or thrombin were used as aggregating agents. Thus, O2 − participate in the aggregatory activity of thrombin but not collagen or ADP and PGI2 or iloprost, by reducing the sensitivity of platelets to thrombin, co-operate with SOD to inhibit thrombin-induced platelet aggregationThe interpretation of the use of SOD in experiments involving endothelium-derived relaxing factor (NO) is discussed

1993 ◽  
Vol 70 (05) ◽  
pp. 834-837 ◽  
Author(s):  
Akira Suehiro ◽  
Yoshio Oura ◽  
Motoo Ueda ◽  
Eizo Kakishita

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.


1981 ◽  
Vol 46 (02) ◽  
pp. 538-542 ◽  
Author(s):  
R Pilo ◽  
D Aharony ◽  
A Raz

SummaryThe role of arachidonic acid oxygenated products in human platelet aggregation induced by the ionophore A23187 was investigated. The ionophore produced an increased release of both saturated and unsaturated fatty acids and a concomitant increased formation of TxA2 and other arachidonate products. TxA2 (and possibly other cyclo oxygenase products) appears to have a significant role in ionophore-induced aggregation only when low concentrations (<1 μM) of the ionophore are employed.Testosterone added to rat or human platelet-rich plasma (PRP) was shown previously to potentiate platelet aggregation induced by ADP, adrenaline, collagen and arachidonic acid (1, 2). We show that testosterone also potentiates ionophore induced aggregation in washed platelets and in PRP. This potentiation was dose and time dependent and resulted from increased lipolysis and concomitant generation of TxA2 and other prostaglandin products. The testosterone potentiating effect was abolished by preincubation of the platelets with indomethacin.


1976 ◽  
Vol 5 (5) ◽  
pp. 306-317
Author(s):  
Ricardo Castillo ◽  
Santiago Maragall ◽  
Javier Alvarez Guisasola ◽  
Francisco Casals ◽  
Juan Profitós ◽  
...  

1997 ◽  
Vol 25 (4) ◽  
pp. S600-S600 ◽  
Author(s):  
BUKHTIAR H. SHAH ◽  
SHEIKH A. SAEED ◽  
GAZALA SHAMIM ◽  
ZAFAR NAWAZ ◽  
ANWAR H. GILANI

1985 ◽  
Vol 53 (02) ◽  
pp. 221-224 ◽  
Author(s):  
Marco Cattaneo ◽  
Maria Teresa Canciani ◽  
Pier Mannuccio Mannucci

SummaryThe effects of the cyclo-oxygenase inhibition on PAF-acether- induced human platelet aggregation and secretion are controversial. We studied the above parameters on citrated platelet-rich plasma of 12 normal subjects before and after the in vivo administration of acetylsalicylic acid (ASA). Individual sensitivities to PAF-acether were highly variable. ASA completely inhibited the platelet secretion induced by low concentrations of PAF-acether, but caused only partial inhibition when platelets were exposed to high concentrations of PAF-acether. The concentration of PAF-acether which overcame the cyclo-oxygenase inhibition varied substantially, depending on the individual sensitivity of the platelets to it. The addition of CaCl2 2 mM to the samples did not affect the extent of the platelet secretion, but increased irreversible aggregation in samples taken both before and after the ASA administration. These data suggest that low concentrations of PAF-acether stimulate the human platelet secretion by activating the cyclo-oxygenase pathway, whereas higher concentrations also trigger other mechanism(s) that suffice to induce human platelet secretion and full aggregation.


2012 ◽  
Vol 7 (7) ◽  
pp. 1934578X1200700 ◽  
Author(s):  
Huei-Ping Dong ◽  
Rei-Cheng Yang ◽  
I-Chun Chunag ◽  
Li-Ju Huang ◽  
Hsing-Tan Li ◽  
...  

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.


1995 ◽  
Vol 77 (5) ◽  
pp. 399-410 ◽  
Author(s):  
Giovanni Anfossi ◽  
Simona Parisi ◽  
Isabella Russo ◽  
Elena M. Mularoni ◽  
Paola Massucco ◽  
...  

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