Nitric oxide (NO) was identified as a physiological mediator of vascular tone in 1987. NO produced by endothelial cells causes vasodilatation and also inhibits platelet aggregation and leucocyte adhesion. Red cells metabolize NO to nitrate but may possibly carry and release, or even produce, NO in hypoxic conditions. NO physiology may have important implications for transfusion medicine, ranging from adverse effects of haemoglobin substitutes to preservation of stored platelets and to detrimental effects of stored red cells.