Inhibition of platelet activation using vitamins.

Some vitamins have beneficial effects on cardiovascular diseases, normalizing platelet function and preventing their excess activation. Anti-platelet vitamins can act directly through inhibitory biochemical pathways in platelets or indirectly by preventing damage to the endothelium or low-density lipoprotein from oxidation. As a rule, each vitamin alone is a weak inhibitor of platelet aggregation.

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.

Platelet activity before and after coronary artery bypass grafting.

The normal response of the platelet can be altered either by increased pro-aggregatory stimuli or by diminished anti-aggregatory substances. Increased platelet activation occurs in the cardiovascular disease states of stable angina pectoris and acute coronary syndromes. Also, cardiac surgery involving cardiopulmonary bypass is associated with extensive contact between blood and synthetic surfaces and leads to a strong activation of platelets.

Potentiation of antiaggregating effect of prostaglandins by alpha-tocopherol and quercetin.

Prostaglandin (PG) I2 (prostacyclin), PGE1 and their analogues are effective inhibitors of platelet aggregation. However, a clinical use of these compounds for the treatment of cardiovascular diseases is restricted due to unwanted side effects. Alpha-tocopherol and quercetin are weak antiplatelet agents.