**Author details**

primary graft failure and remains a significant cause of morbidity and mortality after lung transplantation.[91] Pulmonary microvascular permeability appears to have a bimo‐ dal pattern, peaking at 30 min and 4 h after reperfusion. [92] Mechanical ventilation, car‐ diopulmonary bypass during cardiac surgery and lung resection can also induce

Perioperative acute renal failure is associated with a high incidence of morbidity and mortality. According to the type of surgery, IR injuries in the kidney are direct or indi‐ rect. [97] For example, acute renal failure is the most important complication of remote tissue damage following abdominal aortic surgery. [98] I/R induces renal tubular injuries and contributes to the decrease of glomerular filtration. Recent data suggest that 13% of patients with acute kidney injury (AKI) evolve to end-stage renal disease within 3 years. In the case of patients with preexisting renal disease, the progression to end-stage renal disease rises to 28% within the same period. [98] These results suggest that AKI predis‐ poses to chronic renal complication. I/R reduces blood vessel density and promotes renal fibrosis. The mechanisms mediating vascular loss are not clear but may be related to the

In cardiac surgery and in myocardial ischemia, cell death following I/R has features of apoptosis and necrosis. The loss of cardiomyocytes, which can hibernate in "no reflow" zones, and stunning, led by free radicals and calcium overload, explain the contractile posthypoxic dysfunction. The stunned cardiomyocytes can take several hours and days to recover. Intracellular ionic perturbation favors ventricular arrhythmias, such as ventricular fibrillation, ventricular tachycardia or ventricular extrasystole. [10 ]0 During ischemia, cardiomyocytes express ICAM-1. Neutrophils bind to this receptor and empty the contents of their granules

The mechanisms of I/R-induced brain injury have many similar aspects compared with those of I/R-induced myocardial injury. Many mediators and cytokines upregulated by I/R, such as bradykinin, purine nucleotides, nitric oxide and ROS, increase blood–brain barrier permea‐ bility and induce cerebral edema. [10 ]1 Although leukocyte infiltration into the ischemic brain increases cerebral damage, leukocyte accumulation in the microcirculation reduces reperfu‐

The indirect repercussions of I/R on organs remote from the reperfused site are much more insidious. Neutrophils, complement activation, and massive production of cytokines and chemokines install a proinflammatory state that affects the functioning of other organs. During abdominal aortic surgery, I/R injuries are not only limited to the lower extremities but also cause damage to remote organs such as the lungs, kidneys, heart and bowel. [36],[97],[102- [104] Lung injuries following abdominal aortic aneurysm surgery are characterized by progressive hypoxemia, pulmonary hypertension, decreased lung compliance and nonhydro‐ static pulmonary edema, consistent with adult respiratory distress syndrome. [36],[103] In comparison with surgery, endovascular abdominal aortic aneurysm repair decreases I/R and

I/R-induced-intestinal mucosal, renal and pulmonary dysfunction. [104]

apoptosis and I/R-induced lung injury. [93]-[96]

lack of effective vascular repair responses. [99]

sion and increases the "no reflow" phenomenon.

onto the cells. [54],[55]

26 Artery Bypass

Maximilien Gourdin and Philippe Dubois\*

Department of Anaesthesiology, Université Catholique de Louvain, University Hospital of Mont Godinne, Belgium
