Ischaemia significantly affects the cellular homeostasis (sodium and calcium overload, intracellular acidosis, swelling, cytoskeleton injuries, mitochondrial hypercalcaemia and others). If reperfusion of an organ in ischaemia is essential for its viability and its functional recovery, the arrival of blood oxygen will cause a series of lesions; this is known as the phenomenon of ischaemia–reperfusion. Vasomotricity and the endothelial functions are significantly affected by it. Endothelium-dependent vasodilatation is more affected by ischaemia–reperfusion injuries than vasoconstriction and endothelial-independent vasodilatation. Reactive oxygen species and tumour necrosis factor-α seem to play a major role in this perturbation. Reperfusion also induces an important inflammatory response, characterized by a massive production of free radicals and by the activation of the complement and leucocyte neutrophils. A narrow interaction between activated endothelium and neutrophils will result in a significant concentration of neutrophils activated in the interstitium, where they release many oxygen radicals and many kinds of proteases, which destroy cells and extracellular matrix. This transfer of neutrophils from the intravascular bed to the intestitium involves several families of proteins such as selectins (P-selectin and L-selectin), integrines (intercellular adhesion molecule-1) and immunoglobulins (platelet–endothelial cell adhesion molecule-1). Last, oxidative stress, the production of cytokines and the secondary mitochondrial lesions that occur with reperfusion will induce apoptosis on the level of the parenchyma and the vascular structures. According to the stage of the vascular system considered (small arteries, capillaries or postcapillary veins), the repercussions of ischaemia–reperfusion are identical, but the clinical pictures differ. The proinflammatory state induced by reperfusion continues for several days and can affect the patient's prognosis.