Copyright © European Society of Anaesthesiology. Unauthorized reproduction of this article is prohibited. The impact of ischaemia–reperfusion on the blood vessel Maximilien J. Gourdin a , Bernard Bree b and Marc De Kock b 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-a 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. Eur J Anaesthesiol 26:537–547 Q 2009 European Society of Anaesthesiology. European Journal of Anaesthesiology 2009, 26:537–547 a Department of Anaesthesiology, Universite ´ Catholique de Louvain, University Hospital of Mont Godinne, Yvoir and b Department of Anaesthesiology, Universite ´ Catholique de Louvain, University Hospital Saint-Luc, Brussels, Belgium Correspondence to Maximilien J. Gourdin, MD, Department of Anaesthesiology, Universite ´ Catholique de Louvain, University Hospital of Mont Godinne, Avenue Dr Therrasse 1, 5530 Yvoir, Belgium Tel: +32 81 422111 x 3917; fax: +32 81 423920; e-mail: maximilien.gourdin@uclouvain.be Received 26 March 2008 Revised 30 June 2008 Accepted 3 October 2008 Introduction The reperfusion of an organ in ischaemia is essential for its viability and its functional recovery. But there is a flip side to this coin, the arrival of blood oxygen will cause a series of lesions; this is known as the phenomenon of ischaemia– reperfusion (I/R). Histologically, the restoration of an adequate blood flow to liver or intestines after 3h of ischaemia followed by 1h of reperfusion presents more parenchymatous or mucous membrane necroses than the same organ subjected to 4h of ischaemia alone [1,2]. The arterial clamping/unclamping in vascular surgery, the use of a tourniquet in orthopaedic surgery, cardiac surgery with or without extracorporeal circulation, transplant surgery, haemorrhagic shocks, septicaemia and low blood flow states are only some examples which illustrate daily I/R in clinical practice in the operating theatre. I/R generates an important local inflammatory reaction which affects mainly the organ concerned but can also affect two other organs. In orthopaedic surgery, the use of the tourniquet on the lower limbs affects both the lung and liver [3–5]. A small intestine I/R induces apoptotic and necrotic parenchymatous lesions in pulmonary, renal and cardiac endothelium [6]. Organs with a high capillary density such as the lungs are more sensitive to I/R lesions. A remote I/R such as that of the splanchnic bed or a lower limb in orthopaedic surgery can induce an acute lung injury [6]. Often, these repercussions remain subclinical but can generate a systemic inflammatory response syn- drome or even multiorgan failure and lead to the death of the patient [6]. The vascular system and particularly the endothelium are very sensitive to I/R injuries. The endothelial cells have multiple vital duties; they control vascular tonicity and local blood flow, modulate coagulation and inflammation, intervene in the immune system, control the transfer of micro and macromolecules towards the interstitial region, convert prohormones into active hormones (angiotensin II) and intervene in the formation of new blood vessels. It is thus vital to preserve them. In the heart, the reperfusion- induced endothelial injuries contribute to myocardial depression [7,8]. The effects of I/R on the endothelium can go from the sideration of endothelial function to necrosis. The importance and the frequency of the I/R phenom- enon in clinical practice make its physiopathology of interest to anaesthesiologists. This review proposes to present to clinicians the various stages and mechanisms Review 537 0265-0215 ß 2009 Copyright European Society of Anaesthesiology DOI:10.1097/EJA.0b013e328324b7c2