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PubMed2006

Synergistic effect of ginger and nifedipine on human platelet aggregation: a study in hypertensive patients and normal volunteers.

In this study, we evaluated the synergistic effect of ginger and nifedipine on anti-platelet aggregation in normal human volunteers and hypertensive patients. The results showed that the percentage of platelet aggregation induced by collagen, ADP and epinephrine in hypertensive patients was larger than that in normal volunteers. Either aspirin or ginger could potentiate the anti-platelet aggregation effect of nifedipine in normal volunteer and hypertensive patients. These results suggested that ginger and nifedipine possessed synergistic effect on anti-platelet aggregation. A combination of 1 g ginger with 10 mg nifedipine per day could be valuable for cardiovascular and cerebrovascular complication due to platelet aggregation.

Adenosine Diphosphate↗
PubMed1992

ADP plays an important role in mediating platelet aggregation and cyclic flow variations in vivo in stenosed and endothelium-injured canine coronary arteries.

The goal of this study was to test the hypotheses that endogenous ADP plays an important role in vivo in mediating platelet aggregation and cyclic coronary artery blood flow variations (CFVs) in stenosed and endothelium-injured coronary arteries in an experimental canine model. Anesthetized animals were studied and coronary blood flow velocities monitored by a pulsed Doppler flow probe positioned around the left anterior descending coronary artery. CFVs were established by an external constrictor positioned at sites with injured endothelium. Apyrase, an ADP-removing enzyme, was infused into the left anterior descending coronary artery (0.3-1.8 units/min) 30 minutes or 2 hours after the establishment of CFVs. Complete abolition of CFVs was achieved in 81% (13/16) of dogs with 30-minute CFVs and in 83% (five of six) of dogs with 2-hour CFVs. In other dogs, a potent inhibitor of ADP-induced platelet aggregation, clopidogrel, was administered as a 10 mg/kg i.v. bolus and a 2.5 mg/kg/hr infusion 30 minutes and 3 hours after the establishment of CFVs. This treatment resulted in complete abolition of CFVs in 14 dogs (100%) with either 30-minute or 3-hour CFVs. Epinephrine was infused into some dogs after CFVs had ceased as a result of either apyrase or clopidogrel administration and into some dogs in whom SQ29548, a thromboxane A2 receptor antagonist, had been given when apyrase failed to abolish CFVs. Epinephrine restored CFVs in all dogs treated with apyrase alone, 67% (four of six) of dogs treated with the combination of apyrase and SQ29548, and 29% (two of seven) of dogs treated with clopidogrel. The plasma epinephrine levels required for CFV restoration were 20 times higher than baseline values in dogs receiving apyrase alone, 100 times higher when a combination of apyrase and SQ29548 had been given, and more than 5,000 times higher in dogs receiving clopidogrel. In vitro studies showed that apyrase only inhibited ADP-induced platelet aggregation, whereas clopidogrel not only inhibited ADP-induced platelet aggregation, but also reduced platelet aggregation induced by the thromboxane mimetic U46619 and serotonin. These data suggest that 1) ADP is an important mediator of platelet aggregation and CFVs in vivo and 2) combined inhibition of thromboxane A2 and ADP's effects provides marked protection against CFVs in experimentally stenosed and endothelium-injured canine coronary arteries. These data and our previous observations are consistent with the possibility that specific antagonists of thromboxane A2, serotonin, and ADP, alone and together, may provide substantial protection against platelet aggregation leading to CFVs at sites of endothelial injury and coronary artery stenosis.

Adenosine Diphosphate↗
PubMed1986

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

Platelets are involved in the pathogenesis of vascular disease, and calcium channel blocking agents (CCB) such as nicardipine, are being used in the treatment of such disorders. CCB's are known to have minor anti-platelet actions from studies performed in platelet rich plasma (PRP). Recently it has become possible to study platelet aggregation in whole blood. The effects of nicardipine on whole blood platelet aggregation were studied in-vitro using the Clay-Adams Ultra Flo 100 whole blood platelet counter. Nicardipine inhibited aggregation to 0.5 micrograms/ml collagen, and 0.5 mM arachidonic acid in a dose dependent manner, but had minimal effects on aggregation to 10 microM ADP. Nicardipine also acted synergistically with prostacyclin to inhibit aggregation. The effect of nicardipine on generation of PGI2 and TxA2 from whole blood was studied. Nicardipine did not affect TxA2 production, but significantly increased PGI2 production at high concentration. The effect of nicardipine on vascular PGI2 production was also assessed using umbilical artery rings, but nicardipine had no effect on PGI2 production. This study confirms that CCBs have inhibitory actions on platelet aggregation, and this may be of value in the treatment of vascular disease.

Adenosine Diphosphate↗
PubMed1991

In vitro effects of picotamide on human platelet aggregation, the release reaction and thromboxane B2 production.

We studied the in vitro effects of picotamide (N,N' bis 3 picolyl-4-methoxy-isophthalamide) on human platelet aggregation, the release reaction and the production of thromboxane B2 (TxB2) induced by several platelet agonists. The effects of picotamide were compared to those of acetylsalicylic acid (ASA). Picotamide (0.5 mmol/l) inhibited platelet aggregation, the release of ATP and TxB2 production induced by ADP, arachidonic acid (AA), collagen or the prostaglandin endoperoxide (PE) analogue U46619. ASA (0.5 mmol/l) did not affect platelet aggregation and the release of ATP induced by U46619. Picotamide and ASA inhibited the AA-induced platelet TxB2 production both under stirring and non-stirring conditions, whereas the pure thromboxane A2 receptor antagonist BM13177 (0.5 mmol/l) was inhibitory only under stirring conditions. Since under non-stirring conditions platelet aggregation does not occur, picotamide directly inhibits TxB2 production, whereas BM13177 inhibits the potentiation of TxB2 production due to TxA2/PE-dependent platelet aggregation. Malondialdehyde (MDA) production by unstirred platelets stimulated with AA was not significantly inhibited by picotamide. In conclusion, picotamide inhibits the TxA2/PE-dependent platelet responses to agonists by a double mechanism: (i), TxA2/PE antagonism; (ii) inhibition of thromboxane synthase.

Adenosine Diphosphate↗
PubMed1978

Platelet aggregation in patients with peripheral vascular disease.

Platelet aggregation has been studied in 28 control subjects and 46 patients with peripheral vascular disease. The platelets from the patients with peripheral vascular disease were significantly more sensitive to the aggregating effects of adenosine diphosphate and adrenaline than those from the control group (P less than 0.001). In addition, spontaneous platelet aggregation was observed in vitro in several of the vascular patients; this response was not apparent in the control group. Increased platelet aggregation could add to the vascular impairment in the unoperated subject and might also play a part in premature graft failure. Platelet function studies should perhaps be included as a routine in the assessment of patients with peripheral vascular disease.

Adenosine Diphosphate↗
PubMed1994

A stable leukocyte-derived factor inhibits platelet aggregation.

The effect of human polymorphonuclear leukocyte (PMN)-derived supernatants on platelet aggregation was studied. The results showed that the supernatants produced a concentration-dependent inhibition of the platelet aggregation in response to thrombin. The effect was mainly on the second phase of the aggregation, suggesting that the secretory mechanisms of the platelets are disturbed. The activity of the supernatants was not reduced after treatment with heat (95 degrees C for 30 minutes), extreme pH (pH 12 or pH 2) or protease. In conclusion, human PMNs release a stable non-protein factor that inhibits platelet aggregation.

Biological Factors↗
PubMed1989

Human neutrophils and mononuclear cells inhibit platelet aggregation by releasing a nitric oxide-like factor.

Incubation of neutrophils or mononuclear cells with washed platelets (all prepared from human venous blood) resulted in an inhibition of thrombin-induced platelet aggregation that was dependent on the number of nucleated cells added. The inhibition was potentiated by superoxide dismutase and reversed by oxyhemoglobin. In the case of neutrophils the inhibition was associated with an increase in cGMP, whereas with mononuclear cells both cAMP and cGMP were increased. The inhibitory activity of neutrophils or mononuclear cells was prevented by their preincubation with NG-monomethyl-L-arginine methyl ester. L-Arginine reversed the action of NG-monomethyl-L-arginine methyl ester, whereas D-arginine was ineffective. Preincubation of the cells with catalase or mannitol did not prevent their inhibitory action on platelet aggregation. The inhibition of platelet aggregation was not due to platelet damage or to uptake of thrombin by neutrophils or mononuclear cells. It was overcome by increasing the concentration of thrombin and was absent in cell-free supernatants obtained from a suspension of neutrophils or mononuclear cells or from mixtures of platelets with neutrophils or platelets with mononuclear cells. These data provide evidence for the release of a nitric oxide-like factor from human neutrophils and mononuclear cells. In addition, evidence is provided that, as in stimulated murine macrophages and endothelial cells, the precursor of this factor is L-arginine.

Cyclic AMP↗
PubMed2002

Short-term inhibition of ADP-induced platelet aggregation by clopidogrel ameliorates radiation-induced toxicity in rat small intestine.

Endothelial dysfunction and increased platelet aggregation may be involved in the pathogenesis of normal tissue radiation toxicity. This study assessed clopidogrel, an inhibitor of ADP-induced platelet aggregation, as a modulator of intestinal radiation injury (radiation enteropathy). Rat small intestine was exposed to 21 Gy X-radiation. Clopidogrel (20 mg/kg/day) or vehicle was administered from 2 days before to 10 days after irradiation. Structural radiation injury, neutrophil infiltration, smooth muscle cell proliferation, collagen content, and TGF-beta1 expression were assessed 2 weeks (early phase) and 26 weeks (delayed phase) after irradiation, using quantitative histology and immunohistochemistry, morphometry, and real-time fluorogenic probe RT-PCR. Irradiated intestine exhibited significant histopathologic injury, reduced mucosal surface area, vascular sclerosis, intestinal wall fibrosis, increased collagen content, and increased TGF-beta1 expression. Clopidogrel reduced ADP-induced platelet aggregation by 93% and significantly attenuated the severity of post-radiation vascular sclerosis (p = 0.004 and p = 0.02) and the loss of mucosal surface area (p = 0.0008 and p = 0.003) at both 2 and 26 weeks. Clopidogrel also ameliorated overall histopathologic injury (p = 0.02), relative intestinal collagen content (p = 0.03), and collagen III immunoreactivity levels 2 weeks after irradiation, and caused a borderline reduction in the radiation-induced increase in extracellular matrix-associated TGF-beta immunoreactivity at 26 weeks (p = 0.04). The effects of clopidogrel on steady-state TGF-beta1 mRNA levels and neutrophil infiltration were not statistically significant. Short-term clopidogrel administration affords protection against early and, to a lesser extent, delayed radiation enteropathy. Modulation of platelet aggregation should be subject to further studies as a potential method to increase safety and efficacy of radiation therapy.

Adenosine Diphosphate↗
PubMed1998

Effects of chroman derivatives on platelet aggregation induced by some aggregating agents in rabbits.

1. We synthesized 10 chroman derivatives (CD-1 to CD-10) derived from khellactone, including praeruptorin A and praeruptorin B and examined the effects of these compounds on rabbit platelet aggregation. 2. These compounds exhibited an inhibitory effect on platelet-activating factor (PAF)-induced platelet aggregation and their effects were more potent on PAF-induced platelet aggregation than on adenosine triphosphate (ADP)-, arachidonate (AA)- or collagen-induced platelet aggregation. In particular, (+/-)-cis-5-methoxy-6-methoxycarbonyl-2,2-dimethyl-3,4-ditiglyloxychr oman (CD-6), (+/-)-cis-5-methoxy-6-(2-methoxycarbonylethenyl)-2,2-dimethyl- 3,4-ditiglyloxychroman (CD-8), (+/-)-cis-3,4-diacetoxy-5-methoxy-2,2-dimethyl-6-propylchroman (CD-9) and (+/-)-cis-5-methoxy-2,2-dimethyl-6-propyl-3,4-ditiglyloxychroman (CD-10) showed a moderate inhibition of PAF-induced platelet aggregation. 3. From these findings, it is suggested that compounds with potent PAF antagonist activities have the following features: (i) a tiglyloxy moiety is required at the 3 and 4 positions; and (ii) the methoxy moiety is also required at the 5 position of chroman skeleton in khellactone.

Adenosine Diphosphate↗
PubMed1978

Release of arachidonic acid from human platelets. A key role for the potentiation of platelet aggregability in normal subjects as well as in those with nephrotic syndrome.

Low (nonaggregating) concentrations of collagen that potentiate platelet aggregation did not induce the formation of measurable amount of malondialdehyde (MDA) but released small but significant amounts of radioactivity from 14C-arachidonic acid-labeled platelets. A major portion of the radioactive compounds released by nonaggregating concentrations of collagen existed as arachidonic acid and a minor part as thromboxane B2. The nephrotic syndrome enhances platelet aggregability, and this effect is abolished by correcting hypoalbuminemia in vitro and in vivo by the addition of albumin, which is the main carrier for free fatty acids, including arachidonic acid. Human albumin (fatty acid free) inhibited collagen-induced aggregation, MDA formation, and release of the radioactivity from 14C-arachidonic acid-labeled platelets in normals as well as in those with nephrotic syndrome. These data support our hypothesis that the main mechanism responsible for the potentiation of platelet aggregation is the release of arachidonic acid from platelet membrane phospholipids via the activation of phospholipase A2. Furthermore, enhanced platelet aggregation in the nephrotic syndrome was at least partly attributable to an increased availability of arachidonic acid released secondary to hypoalbuminemia. Albumin inhibits aggregation probably by binding to released arachidonic acid preventing arachidonic acid from being metabolized to potent aggregating substances, endoperoxides and thromboxane A2. The mechanism of release of arachidonic acid may play a key role in the potentiation of platelet aggregability in normals as well as in pathologic conditions such as the nephrotic syndrome.

Albumins↗
PubMed1981

Effect of phosphodiesterase inhibitors on platelet aggregation and tumor metastasis.

Recent studies suggest a relationship of platelet aggregation to metastatic spread of neoplasia. In the present experiment pentoxifylline appears to be a highly effective platelet aggregation inhibitor: a dose-response curve is apparent in monkey between 6 and 24 mg/kg i.v. Besides pentoxifylline significantly reduces metastasis rates in Wilms' tumor and neuroblastoma in rodents: 18 mg/kg significantly increase polyploid Ehrlich ascites tumor cell circulation time; on the contrary it has no effect on metastasis in the NIH renal adenocarcinoma. It is thus possible that platelet factor related blood coagulation processes play a different role in the fate of these tumor cells. This may be related to cell membrane characteristics. Phosphodiesterase inhibitors alter membrane fluidity and cell deformability of cancer cells which may pass the microcirculation easier and are less likely to settle and form metastases. Agents with both platelet aggregation inhibitory and red cell deformability increasing effect may find a place in our therapeutic armamentarium in oncology.

Adenocarcinoma↗
PubMed2005

Vitronectin stabilizes thrombi and vessel occlusion but plays a dual role in platelet aggregation.

The role of vitronectin (Vn) in thrombosis is currently controversial; both inhibitory and supportive roles have been reported. To monitor directly the function of Vn in thrombotic events at the site of vascular injury, we studied Vn-deficient (Vn-/-) and wild-type (WT) control mice with two real-time intravital microscopy thrombosis models. In the mesenteric arteriole model, vessel injury was induced by ferric chloride. We observed unstable thrombi and a significantly greater number of emboli in Vn-/- mice. Vessel occlusion was also delayed and frequent vessel re-opening occurred. In the cremaster muscle arteriole model, vessel injury was induced by a nitrogen dye laser. We observed significantly fewer platelets, lower fibrin content, and unstable fibrin within the thrombi of Vn-/- mice. To define further the role of Vn in thrombus growth, we studied platelet aggregation in vitro. Consistent with our in vivo data, the second wave of thrombin-induced aggregation of gel-filtered platelets was abolished at a low concentration of thrombin in Vn-/- platelets. Interestingly, adenosine diphosphate (ADP)-induced platelet aggregation was significantly increased in Vn-/- platelet-rich plasma (PRP) and this effect was attenuated by adding purified plasma Vn. We also observed increased platelet aggregation induced by shear stress in Vn-/- whole blood. These data demonstrate that Vn is a thrombus stabilizer. However, in contrast to released platelet granule Vn which enhances platelet aggregation, plasma Vn inhibits platelet aggregation.

Adenosine Diphosphate↗
PubMedDate not supplied

Interaction between amitraz and alpha 2-adrenoceptors inhibits epinephrine-induced canine platelet aggregation.

The effect of amitraz, a formamidine insecticide, on [3H]yohimbine binding and aggregation of canine platelets was studied. The time course study of [3H]yohimbine binding to alpha 2-adrenoceptors on canine platelet membranes showed a maximum binding after 45 min at 37 degrees C using 5.25 nM final concentration of radioligand. When maximum binding was reached, amitraz (10(-4) M) was added to inhibit [3H]yohimbine binding. The dose-dependent inhibition of radioligand binding by amitraz was compared with that of chlordimeform, another formamidine insecticide, and clonidine. The IC50 values for clonidine, amitraz and chlordimeform indicated that amitraz was about 5 times less potent than clonidine and 6 times more potent than chlordimeform. Epinephrine (10(-6) M) promoted both primary and secondary aggregation of canine platelets in the presence of 10(-6) M ADP. Both amitraz (3 x 10(-7)-10(-5) M) and clonidine (3 x 10(-7)-10(-6) M) inhibited epinephrine-induced canine platelet aggregation in a dose-dependent manner. These results suggest that amitraz has a direct interaction with alpha 2-adrenoceptors of canine platelets to inhibit epinephrine-induced aggregation.

Animals↗
PubMed2002

Quality control of platelets during storage by the PFA-100: a comparison to platelet aggregation.

BACKGROUND AND OBJECTIVES: The PFA-100 examines platelet function by measuring closure time (CT) when whole blood is passing through a capillary and a filter membrane coated with a collagen/platelet agonist. Termination of the CT is achieved when adhered and aggregated platelets of the passing blood flow occlude the membrane. Two PFA-100 test cartridges are used to measure the CT of citrated whole blood; either the collagen/ADP (PCA) or the collagen/ epinephrine (PCE). We investigated the applicability of the PFA-100 test system for quality control of platelet concentrates in comparison with platelet aggregometry. MATERIALS AND METHODS: For platelet aggregation, the combination of ADP (100 microM/l) and collagen (20 microg/ml) were used as agonists (ADP/COL). In our test system, 25 microl epinephrine (10(-3) M) were added to the PCA cartridge (CT: PCAE) and 25 microl ADP (100 microM/l) to the PCE cartridge (CT: PCEA), respectively. Red blood cells from a blood group 0 donor were adjusted to a hematocrit of 43% using platelet rich plasma (8 x 10(5)/microl) of the respective platelet concentrate. Fourteen irradiated and non-irradiated platelet concentrates were examined on days 0, 3 and 5 after platelet preparation. Swirling without a scoring system and mean platelet volume (MPV) were also tested. Statistical analyses were performed by Pearson's range coefficient, the Mann and Whitney test, and the Wilcoxon test. RESULTS: Swirling was seen in all platelet concentrates. Mean platelet volume was normal during the whole observation period like the PCAE in non-irradiated products. Only the PCAE showed finite CTs during the whole storage time. Consequently, further testing was performed exclusively with the PCAE. Weak but significant correlations could be found between the PCAE and ADP/COL (r = -0.53 for non-irradiated platelet products, r = -0.62 for irradiated platelet products, p < or = 0.0001). Platelet function significantly decreased to around 60% of the initial value in the PCAE on day 5 of storage, ADP/COL decreased to 35% of maximum amplitude. A further decrease of approximately 10% was observed in the irradiated products, a fact which was significant in the PCAE. Only in the irradiated platelet products did MPV show a weak but significant correlation with the PCAE (r = 0.45, p = 0.002). CONCLUSION: Functional features of platelets from platelet concentrates characterized by ADP/COL induced aggregation can also be measured by the PFA-100. Yet, it has a higher sensitivity to platelet lesions induced by gamma-radiation. Further clinical studies will be necessary to determine whether PFA-measurements meet the quality criteria of MPV or swirling, or is superior in predicting in vivo viability. The relatively high cost of the test cartridge remains an obstacle for routine use.

Adenosine Diphosphate↗
PubMed1992

Effects of a sustained thromboxane synthase inhibition on exercise-induced changes in eicosanoid formation, catecholamine concentration, and platelet aggregation in humans.

In an effort to characterize an interaction between the eicosanoids and sympathoadrenal system on platelet aggregation, we tried to determine if a sustained thromboxane A2 (TXA2) synthase inhibition would modulate changes in eicosanoid formation, catecholamine concentration, and platelet aggregation induced by a physical stress. We measured thromboxane B2 (TXB2), 11-dehydro-TXB2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), norepinephrine, and epinephrine in vivo and platelet aggregation ex vivo before and after a treadmill exercise with and without the oral doses (400 mg twice daily for 7 days) of a new selective TXA2 synthase inhibitor (DP-1904) in nine healthy male subjects. The exercise tests performed on the pretreatment day (day 0) and posttreatment day (day 7) gave a similar result. DP-1904 caused a decrease in serum and urinary TXB2 and urinary 11-dehydro-TXB2 (p less than 0.001 to p less than 0.01) and an increase in serum 6-keto-PGF1 alpha (p less than 0.001 to p less than 0.05) throughout the dosing interval on days 4 and 7. Despite the drug effect on eicosanoid formation at rest and after exercise, the exercise-induced plasma norepinephrine and epinephrine concentrations did not differ between days 0 and 7. The 7-day treatment decreased (p less than 0.01) platelet aggregation induced both by adenosine diphosphate and by collagen at rest. However, the exercise increased (p less than 0.01) platelet aggregation by the two aggregators, resulting in the disappearance of the drug-induced antiaggregatory effects observed at rest. The treatment with a TXA2 synthase inhibitor does not appear to attain the antithrombotic action during an exercise despite the occurrence of a sustained endoperoxide shunting.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Identification of a platelet-aggregating factor of murine colon adenocarcinoma 26: Mr 44,000 membrane protein as determined by monoclonal antibodies.

The interaction between platelets and tumor cells plays an important role in the hematogenous spread of certain malignant cancers. We found that metastatic clones of murine colon adenocarcinoma 26 induced platelet aggregation in a membrane protein-dependent manner. Two monoclonal antibodies (mAbs) of IgG2a class were generated against a highly metastatic colon 26 clone, NL-17. These two mAbs, designated 8F11 and 20A11, showed a two-fold higher level of NL-17 binding than a low metastatic clone, NL-14, which possesses low platelet-aggregating ability. Both mAbs retarded platelet aggregation induced by NL-17. Western blot analysis showed that both mAbs recognized the same Mr 44,000 membrane protein as antigen under reducing conditions. Trypsin treatment of NL-17 diminished the ability of the cells to induce platelet-aggregation and resulted in a decrease in the reactivity of the cells to 8F11. These results suggest that the Mr 44,000 membrane protein recognized by the two mAbs is a platelet-aggregating factor of colon 26 cells.

Adenocarcinoma↗
PubMed1986

Platelet aggregation inhibitors from Agkistrodon acutus snake venom.

Among all the purified components from A. acutus venom, including ADPase, 5'-nucleotidase, phospholipase A2 and fibrinogenases, only the venom ADPase (50-100 micrograms/ml) shows marked inhibitory action on ADP (10 microM)-, collagen (10 micrograms/ml)- and sodium arachidonate (100 microM)-induced platelet aggregations of rabbit platelet-rich plasma. The venom 5'-nucleotidase (100 micrograms/ml) inhibited ADP-induced platelet aggregation by 31 +/- 4% (n = 4, P less than 0.05). Fibrinogenolytic enzymes (fractions I and IX, 100 micrograms/ml) did not significantly inhibit platelet aggregation induced by ADP (10 microM), collagen (10 micrograms/ml) or sodium arachidonate (100 microM). However, when the fibrinogenase (fraction IX, 100 micrograms/ml) was preincubated with platelet-rich plasma for 30 min it inhibited collagen (20 micrograms/ml)- and ADP (10 microM)-induced platelet aggregations by 34 +/- 9% (n = 4, P less than 0.05) and 35 +/- 6% (n = 4, P less than 0.05), respectively. The phospholipase A2 (100 micrograms/ml) did not affect platelet aggregation. The venom ADPase is a single chain polypeptide with a molecular weight of 94,000. The specific ADPase activity is estimated to be 4.3 mu moles Pi/min/mg of protein. It also possesses phosphodiesterase and weak 5'-nucleotidase activities.

5'-Nucleotidase↗
PubMed2004

Mechanism of activation of ADP-induced platelet aggregation under the influence of oxidatively modified fibrinogen.

For evaluation of the mechanisms underlying the effect of oxidized fibrinogen on platelet aggregation we studied ADP-induced platelet aggregation in the presence of UV-oxidized fibrinogen and inhibitors of major enzymes of platelet activation. Cyclooxygenase inhibitor acetylsalicylic acid, protein kinase C inhibitor H7, and to a lesser extent, protein tyrosine kinase inhibitor genistein suppressed ADP-induced platelet aggregation. In the presence of oxidized fibrinogen the degree of suppression was lower than in the presence of nonoxidized fibrinogen. Phospholipase C inhibitor U73122 markedly suppressed platelet aggregation in the presence of oxidized and nonoxidized fibrinogen. It can be hypothesized that oxidized fibrinogen activates platelets by modulating activity of the key signal component phospholipase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗