The interplay between platelet and vessel-wall mediators in coronary artery occlusion.
Myocardial infarction (MI) is associated with platelet aggregation and coronary vasospasm. Endogenous mediators produced by platelets and the vessel wall alter platelet function and smooth muscle tone and may be involved in the infarctive process. The synthesis and actions of these mediators is largely determined by interactions between platelets and the vessel-wall. MI occurs at sites of endothelial cell damage where the balance of mediators is shifted in favour of aggregation and vasospasm. Therapeutic intervention should aim at restoring the balance of mediators, and this will involve manipulation of endothelium-derived nitric oxide or its intracellular second messengers.
Vallance
P
P
Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London, UK.
D001685:Biological Factors / Q000502:physiology; D001792:Blood Platelets / Q000502:physiology*; D003329:Coronary Vasospasm / Q000097:blood / Q000503:physiopathology*; D006801:Humans; D009569:Nitric Oxide
D001685:Biological Factors; D009569:Nitric Oxide