Glucose impairs aspirin inhibition in platelets through a NAD(P)H oxidase signaling pathway.

Hyperglycemia has been suggested to play a role in the increased platelet resistance to antiplatelet therapy in patients with diabetes mellitus. Exposure to high glucose impairs platelet inhibition by aspirin. It has been found that antioxidant agents reduce the effect of glucose, confirming the involvement of reactive oxygen species (ROS) in the effect of glucose.

Lactate is a possible mediator of the glucose effect on platelet inhibition.

Abstract Glucose has been found to impair the inhibition of platelets with aspirin and alter the basal activity of nitric oxide synthase (NOS) in platelets. The aim of this work was to study the effects of glucose on the inhibitory pathways in activated platelets. A short-term incubation of glucose impaired the inhibition of platelet aggregation induced by agents activating an NOS-dependent pathway, such as l-arginine, adenosine and α-tocopherol.

Short-term exposure of platelets to glucose impairs inhibition of platelet aggregation by cyclooxygenase inhibitors.

Aspirin treatment reduces cardiovascular events and deaths in high-risk non-diabetic patients, but not in patients suffering from diabetes. In these patients, hyperglycemia has been found to cause reduced platelet sensitivity to aspirin. It is supposed that long-term exposure of platelets to glucose leads to non-enzymatic glycosylation and impairs aspirin inhibition of platelet aggregation.

Effect of vitamin B(6) vitamers on platelet aggregation.

The vitamers of vitamin B(6) inhibit platelet aggregation. However, their effect is weak when used separately. After the supplementation of one vitamer, the concentrations of the other ones also increase in plasma due to the interconversion of vitamin B(6) forms.

Blood plasma influences anti-aggregatory potency of prostaglandins: effect of albumin.

The anti-aggregatory effects of prostaglandins (PGs) were compared in platelet-rich plasma (PRP) with that in washed platelets (WP). PGE(1), 13,14-dihydro-PGE(1), 5,6-dihydro-PGE(3) and ethyl ester of PGE(1) had the same potency in both platelet preparations. Iloprost was significantly more potent in WP compared to PRP, while 5,6-trans-PGE(2) and PGE(3) had higher potency in PRP than in WP.