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PubMed1985

Correlation between migraine and circulating platelet aggregates.

We studied platelet aggregates, by Wu and Hoak's technique, in 73 patients (49 F and 24 M), aged 14-61 (mean age 50.4 +/- 12.2) with migraine. Platelet aggregates were expressed as Platelet Aggregate Ratio (PAR). We consider as pathological PAR values lower than 86. Mean PAR value of migraine patients (78.3 +/- 8.68 SD) was significantly lower (p less than 0.001) than that of 90 control subjects (95.4 +/- 6.15 SD). Normal PAR values were found only in 27.4% of the migraine patients. The patients were divided according to the interval from the last attack: 17 patients were studied in the 1st week (PAR = 73.76 +/- 7.6 SD; 5.8% of the values in the normal range), 15 in the 2nd week (76.6 +/- 7.02 SD; 13.3% of the values in the normal range) and 41 between 15th and 30th day (80.78 +/- 8.78 SD; 29.6% of the patients in the normal range). The mean PAR value of the patients studied during the first week was significantly lower (p less than 0.01) than that of the patients studied between 15th and 30th day. No significant differences were found between the patients with classical, common and complicated migraine.

Adolescent↗
PubMed1982

Normal platelet aggregation in myotonic dystrophy.

In 18 patients with myotonic dystrophy, spontaneous aggregation and platelet aggregation induced by thrombin, adenosine diphosphate and epinephrine were compared with normal aggregation patterns. In 17 of the 18 patients the results were not significantly different from normal. In 1 patient spontaneous aggregation and hypersensitive platelets were found. These results are in disagreement with earlier reports on a specific hypersensitivity to epinephrine in myotonic dystrophy. Neither the clinical data (myotonia, paresis) nor the laboratory data (creatine kinase, myoglobin, immunoglobulin G) were correlated with the platelet aggregations.

Adenosine Diphosphate↗
PubMed1985

Highly efficient induction of human platelet aggregation in heparinized platelet-rich plasma by diadenosine triphosphate (Ap3A).

Diadenosine triphosphate (Ap3A), which is a releasable dinucleotide of human platelets, induces platelet aggregation when added to heparinized platelet-rich plasma. The concentration dependence of the dinucleotide is similar to ADP. This finding is fully compatible with our recent report of the low potency of Ap3A in citrated platelet-rich plasma relative to ADP. The aggregatory effect of Ap3A in heparinized versus citrated plasma is reflected in the corresponding rates of Ap3A degradation. In citrated plasma, the hydrolysis of Ap3A is drastically slowed down because the hydrolase needs divalent metal ions. The results strongly support the assumption that the aggregatory effect of Ap3A is mediated by the enzymatic hydrolysis of Ap3A which generates ADP as the ultimate stimulus.

Adenine Nucleotides↗
PubMed1988

Endothelium-derived relaxing factor inhibits platelet aggregation in human whole blood in vitro and in the rat in vivo.

Carbachol (0.03-10 microM) or histamine (0.06-10 microM) challenge of indomethacin-pretreated rat aortic rings inhibited ADP-induced aggregation of platelets suspended in anticoagulated human whole blood. The maximum inhibition of platelet aggregation achieved with either drug was approximately 50%. No such inhibition was observed in rat aortic rings rubbed to remove endothelial cells or in intact vessels preincubated with nordihydroguaiaretic acid (NDGA, 10 microM), mepacrine (10 microM) or methylene blue (100 microM). Intravenously (i.v.) injected carbachol (0.5-5 micrograms/kg) also inhibited ADP-induced accumulation of 111indium-labelled platelets in the pulmonary circulation of urethane-anaesthetised rats. This effect of carbachol was inhibited by i.v. injected methylene blue (10 mg/kg) but unaffected by indomethacin (3 mg/kg) or hexamethonium (10 mg/kg) suggesting that PGI2 or adrenaline release did not account for the inhibition of platelet activation observed. Similarly, the platelet inhibitory effect of carbachol in vivo was not related to increased pulmonary vascular blood flow (assessed by accumulation of 111indium-labelled erythrocytes) or blood fibrinolytic activity (measured by euglobulin clot bioassay). The present results suggest that endothelium-derived relaxing factor or a like substance inhibits human platelet aggregation in vitro and rat platelet aggregation in vivo.

6-Ketoprostaglandin F1 alpha↗
PubMed1979

Platelet aggregation and aggregation inhibition by different antiglobulins and antiglobulin complexes from sera of patients with rheumatoid arthritis.

Antiglobulin complexes were isolated from rheumatoid arthritis (RA) sera in order to investigate their ability to aggregate human platelets and to influence platelet aggregation induced by heat-aggregated IgG. Eleven of 38 seropositive RA sera showed a significant platelet aggregation (PA) titer as compared to 40 normal control sera. No correlation was observed between sheep T cell agglutination titers and PA titers of individual sera. Ten of 22 RA antiglobulin preparations containing IgG, IgM, and IgA antiglobulins and antiglobulin complexes also showed positive PA tests. Such preparations were able to inhibit PA brought about by heat-aggregated human IgG. When IgG and IgM antiglobulins were tested separately, only IgM antiglobulins showed this inhibitory effect, whereas IgG antiglobulins were inactive. Neither IgG nor IgM antiglobulins induced PA alone. Reassociated IgG antiglobulin complexes consisting of carefully prepared IgG and isolated IgG antiglobulins were able to induce PA. Platelet aggregation by RA sera was thus shown to be due to IgG antiglobulin complexes present in the sera. It can be concluded from these experiments that the composition of antiglobulin complexes in individual sera comprised of antiglobulins of different classes and IgG "antigen" is responsible for PA results in vitro. In pathophysiologic terms, the reaction of IgG antiglobulin complexes with thrombocytes in vivo may be an important step in the chain of events leading to generalized vascular damage and deposition of immune complexes in vessel walls which is thought to be responsible for the development of generalized vasculitis in RA.

Antibodies, Anti-Idiotypic↗
PubMed1986

Defective platelet aggregation induced by platelet activating factor in myeloproliferative disorders: deficiency of an aspirin-independent mechanism?

Platelets from 6 out of 10 patients with myeloproliferative disorders showed only a single reversible wave of aggregation when challenged with platelet activating factor (PAF). Preexposure to subthreshold concentrations of adrenaline resulted in a full irreversible response to PAF. Aspirin, however, removed this synergism. In the remaining 4 patients, PAF induced a full response but aspirin abolished the synergism with adrenaline in 2 of them. In platelets from all controls aspirin failed to abolish the synergism between PAF and adrenaline. It is suggested that patients with myeloproliferative disorders lack - to varying degrees - an aspirin-independent mechanism which amplifies the primary response to PAF. Such a mechanism could involve the products of arachidonic acid metabolism catalyzed by lipoxygenase.

Adult↗
PubMed1999

Protein disulphide isomerase mediates platelet aggregation and secretion.

Platelet surface thiols and disulphides play an important role in platelet responses. Agents that reduce disulphide bonds expose the fibrinogen receptor in platelets and activate the purified glycoprotein (GP) IIbIIIa receptor. Protein disulphide isomerase (PDI), an enzyme that rearranges disulphides bonds, is found on the platelet surface where it is catalytically active. We investigated the role of PDI in platelet responses using (1) rabbit anti-PDI IgG specific for PDI, (2) a competing substrate (scrambled ribonuclease A), and (3) the PDI inhibitor, bacitracin. Fab fragments of the rabbit anti-PDI IgG inhibited platelet responses to the agonists tested (ADP and collagen), whereas Fab fragments prepared identically from normal rabbit IgG had no inhibitory effect. Scrambled ribonuclease A blocked platelet aggregation and secretion, but native ribonuclease A did not. When biphasic platelet aggregation was examined using platelets in citrated plasma, the principle effect of bacitracin was on second phase or irreversible aggregation responses and the accompanying secretion. Using flow cytometry and an antibody specific for activated GPIIbIIIa (PAC-1), the rabbit anti-PDI Fab fragments substantially inhibited activation of GPIIbIIIa when added before, but not after, platelet activation. In summary, we have demonstrated that protein disulphide isomerase mediates platelet aggregation and secretion, and that it activates GPIIbIIIa, suggesting this receptor as the target of the enzyme.

Animals↗
PubMed1981

Defective platelet aggregation and increased platelet turnover in patients with myelofibrosis and other myeloproliferative diseases.

In 9 patients with myeloproliferative diseases (MPD) (6 with myelofibrosis, MF, 1 with Ph1 positive chronic granulocytic leukaemia, CGL, 1 with primary eosinophilia, PE, 1 with pre-leukaemia syndrome, preL) collagen, epinephrine, and ADP-induced aggregation, N-ethylmaleimide-induced malondialdehyde (MDA) production, beta-thromboglobulin (beta-TG) plasma levels, and platelet turnover were studied. Collagen-induced aggregation was found to be normal in 7 patients, absent in 1, and reduced in 1. In all but 3 patients, aggregation with ADP was markedly reduced. Epinephrine-induced aggregation was decreased in 7 patients. No difference was found between mean MDA production in MPD (3.21 +/- 0.50 nmol/10(9) PLTs) and in control group of 21 normal subjects (3.04 +/- 0.26 nmol/10(9) PLTs). Mean beta-TG levels were significantly higher (P less than 0.01) in MPD patients (165.00 +/- 28.29 ng/ml) than in healthy controls (81.76 +/- 14.63 ng/ml). Mean platelet production half-time was significantly shorter in MPD (2.48 +/- 0.24 d) than in the control group (3.43 +/- 0.17 d), after adjustment for age by covariance analysis (P less than 0.005). Our data do not indicate an abnormal prostaglandin synthesis and are consistent with the hypothesis that a disseminated intravascular platelet aggregation might take place in MPD patients.

Adult↗
PubMed1995

The effect of streptozocin-induced diabetes on platelet aggregation as determined by impedance aggregometry and platelet secretion: a possible role for nitric oxide.

Previous studies from our laboratory showed that diabetes increases platelet aggregation in rats, but only in washed platelets. In the present study, we evaluated platelet aggregation coupled with adenosine triphosphate (ATP) release in normal and diabetic rats using a whole blood electrical aggregometer. Additionally, we investigated the role of endothelium-derived relaxing factor, or nitric oxide, in the platelet reactivity in diabetic rats. Rats were made diabetic using streptozocin, 55 mg/kg. After 1 month the rats were anesthetized, and arterial blood samples were collected directly into sodium citrate solution 3.8%. Platelet counts and mean platelet volumes were determined. Platelet aggregation, disaggregation, and ATP release in response to adenosine diphosphate (ADP), collagen, and arachidonic acid were measured. Platelet aggregation in response to ADP, collagen, and arachidonic acid was not different in diabetic rats when compared with that in controls. However, ATP release in response to ADP was significantly increased in diabetic rats. Platelets from diabetic animals were significantly larger than those of controls. Nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, decreased platelet aggregation in response to ADP in the normal animals, but not in the diabetic animals. However, arginine-induced nitric oxide production decreased platelet aggregation and enhanced the occurrence of disaggregation in platelets from both normal and diabetic rats. From these studies, we conclude that platelet aggregation in diabetic rats is not different using whole blood electrical aggregation, but platelet ATP secretion is significantly enhanced. Additionally, nitric oxide may modulate the platelet aggregation, disaggregation, and ATP secretory response. However, it does not appear to be a major factor in the altered aggregation responses in diabetic rats.

Adenosine Diphosphate↗
PubMed1982

Inhibitors of blood platelet aggregation. Activity of some 1H-benz[de]isoquinolinecarboximidamides on the in vivo blood platelet aggregation induced by collagen.

A series of 33 1H-benz[de]isoquinolinecarboximidamides has been prepared and tested in the rat after intraperitoneal (ip) and/or oral (po) administration for their ability to inhibit the in vivo blood platelet aggregation induced by collagen. In this aggregation test, a considerable number of active compounds were found. Fourteen compounds were active when administered in [0.2 (mmol/kg)/day], five of which also exhibited significant po activity. One compound was toxic after ip administration but was found to be active after po administration without apparent toxicity. It is thought that the solubility of the drug in water is an important factor for the resorption after oral administration and, hence, for its oral activity.

Animals↗
PubMed2002

Occupancy of glycoprotein IIb/IIIa by B-6 vitamers inhibits human platelet aggregation.

Vitamin B-6 inhibits platelet aggregation. However, the effect of the occupancy of GPIIb/IIIa, a major receptor responsible for aggregation on platelet membranes, by B-6 vitamers on platelet aggregation is unknown. This study was carried out to quantify GPIIb/IIIa occupancy in platelets treated with B-6 vitamers [pyridoxal-5-phosphate (PLP); pyridoxal (PL); pyridoxine (PN); pyridoxamine (PM)], using a monoclonal antibody-based assay, by flow cytometry. Antibody binding was compared with inhibition of platelet aggregation. PLP, PL, PN and PM occupied GPIIb/IIIa with dissociation constants of 1.83 +/- 1.15, 19.43 +/- 7.86, 3.63 +/- 1.67 and 10.89 +/- 2.93 mmol/L, respectively. Occupancy of GPIIb/IIIa by the four B-6 vitamers was negatively correlated with platelet aggregation (r = -0.90 to -0.94, P < 0.001). The concentrations of the four B-6 vitamers that inhibited maximal platelet aggregation were in the order of PLP < PN or =80% of the GPII/IIIa receptor. Platelet aggregation was inhibited by B-6 vitamers via the occupancy of GPIIb/IIIa with the potency of PLP > PN > PM > PL.

Humans↗