Pathophysiology, Clinical Manifestations, and Prevention of Ischemia-Reperfusion Injury

ISCHEMIA contributes to the pathophysiology of many conditions faced by anesthesiologists, including myocardial infarction, peripheral vascular insufficiency, stroke, and hypovolemic shock. Although restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury, reperfusion per se may augment tissue injury in excess of that produced by ischemia alone. For example, the histologic changes of injury after 3 h of feline intestinal ischemia followed by 1 h of reperfusion are far worse than the changes observed after 4 h of ischemia alone. Cellular damage after reperfusion of previously viable ischemic tissues is defined as ischemia–reperfusion (I-R) injury. Ischemia–reperfusion associated with thrombolytic therapy, organ transplantation, coronary angioplasty, aortic cross-clamping, or cardiopulmonary bypass results in local and systemic inflammation. If severe enough, the inflammatory response after I-R may result in the systemic inflammatory response syndrome or multiple organ dysfunction syndrome (MODS), which account for 30–40% of the mortality in tertiary referral intensive care units. Thus, I-R injury may extend beyond the ischemic area at risk to include injury of remote, nonischemic organs.