AZD6140 exhibited greater mean inhibition of platelet aggregation than a standard regimen of clopidogrel in ACS patients. In addition, AZD6140 further suppressed platelet aggregation in clopidogrel pretreated patients.
SummaryPlatelet behaviour was studied throughout pregnancy in a group of women who remained normotensive and a group with essential hypertension (EHT). Women who developed pregnancy-induced hypertension (PIH) were also studied together with a group of non-pregnant female controls. We determined the sensitivity of platelets to arachidonic acid (AA) and determined the effects of dazoxiben, a thromboxane synthetase inhibitor, on AA-induced platelet behaviour.A marked increase in platelet reactivity was evident in all three groups throughout pregnancy; platelets became more sensitive to AA and less sensitive to the inhibitory effects of dazoxiben. The change was apparent as early as 16 weeks gestation. In normotensive pregnancy and in EHT platelet behaviour had returned to normal six weeks after delivery. Platelets from women who developed PIH were more sensitive to AA than those from the other pregnant women and platelet reactivity had not returned to normal six weeks after delivery.The results indicate that alterations in platelet behaviour may contribute to the vascular complications that are known to be associated with pregnancy and with PIH in particular.
Summary. Adenosine diphosphate (ADP) released into blood induces platelet aggregation and contributes to hemostasis and thrombosis. Released ATP can also induce platelet aggregation and there is evidence that blood leukocytes and also erythrocytes play important roles in this. Rapid metabolism of ADP and ATP by endothelial cells is important in protecting platelets from their effects. Here we have performed a systematic investigation of adenine nucleotide metabolism in human blood and the involvement of blood cells. Conversion of ATP to ADP in blood was due almost exclusively to the presence of leukocytes; plasma, platelets and erythrocytes made little or no contribution. Mononuclear leukocytes (MNLs) and polymorphonuclear leukocytes (PMNLs) were equally effective. Conversion of ADP to AMP was also promoted by leukocytes, with no involvement of platelets or erythrocytes. Some ADP was also converted to ATP in blood, apparently via an enzyme present in plasma, but ATP was then rapidly removed by the leukocytes. Conversion of AMP to adenosine occurred via a plasma enzyme with little or no contribution from any cellular element. As expected, in blood the adenosine produced was removed very rapidly by erythrocytes and then converted to inosine and then hypoxanthine. In the absence of erythrocytes plasma supported only a slow conversion of adenosine to inosine and hypoxanthine, which was not influenced by platelets or leukocytes. This study has demonstrated that leukocytes and erythrocytes play a major role in adenine nucleotide metabolism in blood and that these cells, as well as endothelial cells, may be important determinants of the effects of ATP and ADP on platelets.
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